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  • 1
    Online Resource
    Online Resource
    Karyomorphology of 〈i〉Curculigo janarthanamii〈/i〉 (Hypoxidaceae): An Important Medicinal Plant from Maharashtra, India
    International Society of Cytology ; 2019
    In:  CYTOLOGIA Vol. 84, No. 1 ( 2019-3-25), p. 85-87
    Details
    In: CYTOLOGIA, International Society of Cytology, Vol. 84, No. 1 ( 2019-3-25), p. 85-87
    Type of Medium: Online Resource
    ISSN: 0011-4545 , 1348-7019
    URL: Article
    DOI: 10.1508/cytologia.84.85
    Language: English
    Publisher: International Society of Cytology
    Publication Date: 2019
    detail.hit.zdb_id: 2394293-9
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  • 2
    Online Resource
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    Karyomorphology of a Critically Endangered Species 〈i〉Vateria indica〈/i〉 L. (Dipterocarpaceae) from India
    International Society of Cytology ; 2020
    In:  CYTOLOGIA Vol. 85, No. 2 ( 2020-6-25), p. 123-126
    Details
    In: CYTOLOGIA, International Society of Cytology, Vol. 85, No. 2 ( 2020-6-25), p. 123-126
    Type of Medium: Online Resource
    ISSN: 0011-4545 , 1348-7019
    URL: Article
    DOI: 10.1508/cytologia.85.123
    Language: English
    Publisher: International Society of Cytology
    Publication Date: 2020
    detail.hit.zdb_id: 2394293-9
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  • 3
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    Online Resource
    Hypothalamic paraventricular nucleus mediates sodium-induced changes in cardiovascular and renal function in conscious sheep
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 297, No. 1 ( 2009-07), p. R185-R193
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 297, No. 1 ( 2009-07), p. R185-R193
    Abstract: The contribution of the paraventricular nucleus of the hypothalamus (PVN) in mediating cardiovascular, renal, hormonal, and sympathetic nerve responses to increased cerebrospinal fluid (CSF) [Na + ] was investigated in conscious sheep. Intracerebroventricular hypertonic NaCl (0.5 mol/l, 20 μl/min for 60 min) increased arterial blood pressure [AP; +13.4 (sd 2.0) mmHg, P 〈 0.001] and central venous pressure [CVP; +2.8 (sd 1.3) mmHg, P 〈 0.001], but did not significantly change heart rate or cardiac output ( n = 6). Elevated CSF [Na + ] also lowered plasma ANG II levels [−3.3 (sd 1.6) pmol/l, P = 0.004] and increased creatinine clearance [+31.5 (sd 32.7) ml/min, P = 0.03] and renal sodium excretion [+9.2 (sd 9.2) mmol/h, P = 0.003] . Lidocaine injection (1 μl, 2%) into the PVN prior to the ICV infusion had no apparent effect per se, but it abolished the AP, CVP, creatinine clearance, and ANG II responses to hypertonic NaCl, as well as reducing the increase in renal sodium excretion ( n = 6). Subsequent studies were performed in conscious sheep with chronically implanted electrodes for measurement of renal sympathetic nerve activity (RSNA). The effects of ICV hypertonic NaCl on AP and RSNA were measured before and after PVN-injection of glycine (250 nmol in 500 nl artificial CSF). ICV NaCl increased AP and decreased RSNA ( P 〈 0.001). These effects were significantly reduced by glycine ( P = 0.02–0.001, n = 5). Saline injected into the PVN ( n = 5) or lidocaine injected outside the PVN ( n = 6) had no effect on the response to ICV hypertonic NaCl. These results indicate that the PVN is an important mediator of cerebrally induced homeostatic responses to elevated sodium concentration/hyperosmolality.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00058.2008
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477297-8
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  • 4
    Online Resource
    Online Resource
    Role of endothelin-1 in mediating changes in cardiac sympathetic nerve activity in heart failure
    American Physiological Society ; 2016
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 310, No. 1 ( 2016-01-01), p. R94-R99
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 310, No. 1 ( 2016-01-01), p. R94-R99
    Abstract: Heart failure (HF) is associated with increased sympathetic nerve activity to the heart (CSNA), which is directly linked to mortality in HF patients. Previous studies indicate that HF is associated with high levels of plasma endothelin-1 (ET-1), which correlates with the severity of the disease. We hypothesized that blockade of endothelin receptors would decrease CSNA. The effects of intravenous tezosentan (a nonselective ET A and ET B receptor antagonist) (8 mg·kg −1 ·h −1 ) on resting levels of CSNA, arterial pressure, and heart rate were determined in conscious normal sheep ( n = 6) and sheep with pacing-induced HF ( n = 7). HF was associated with a significant decrease in ejection fraction (from 74 ± 2% to 38 ± 1%, P 〈 0.001) and a significant increase in resting levels of CSNA burst incidence (from 56 ± 11 to 87 ± 2 bursts/100 heartbeats, P 〈 0.01). Infusion of tezosentan for 60 min significantly decreased resting mean aterial pressure (MAP) in both normal and HF sheep (−8 ± 4 mmHg and −4 ± 3 mmHg, respectively; P 〈 0.05). This was associated with a significant decrease in CSNA (by 25 ± 26% of control) in normal sheep, but there was no change in CSNA in HF sheep. Calculation of spontaneous baroreflex gain indicated significant impairment of the baroreflex control of HR after intravenous tezosentan infusion in normal animals but no change in HF animals. These data suggest that endogenous levels of ET-1 contribute to the baseline levels of CSNA in normal animals, but this effect is absent in HF.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00205.2015
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2016
    detail.hit.zdb_id: 1477297-8
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  • 5
    Online Resource
    Online Resource
    Mechanisms underlying the increased cardiac norepinephrine spillover in heart failure
    American Physiological Society ; 2018
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 315, No. 2 ( 2018-08-01), p. H340-H347
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 315, No. 2 ( 2018-08-01), p. H340-H347
    Abstract: Patients with heart failure (HF) have increased levels of cardiac norepinephrine (NE) spillover, which is an independent predictor of mortality. We hypothesized that this increase in NE spillover in HF depends not only on increases in sympathetic nerve activity (SNA) but also on changes in the mechanisms controlling NE release and reuptake. Such changes would lead to differences between the increases in directly recorded SNA and NE spillover to the heart in HF. Experiments were conducted in conscious sheep implanted with electrodes to record cardiac SNA (CSNA). In addition, arterial pressure and cardiac NE spillover were determined. In HF, the levels of both CSNA (102 ± 8 vs. 45 ± 8 bursts/min, P 〈 0.05) and cardiac NE spillover (21.6 ± 3.8 vs. 3.9 ± 0.8 pmol/min, P 〈 0.05) were significantly higher than in normal control animals. In HF, baroreflex control of cardiac NE spillover was impaired, and when CSNA was abolished by increasing arterial pressure, there was no reduction in cardiac NE spillover. A decrease in cardiac filling pressures in the HF group led to a significant increase in CSNA, but it significantly decreased cardiac NE spillover. In HF, the levels of cardiac NE spillover were enhanced above those expected from the high level of SNA, suggesting that changes in mechanisms controlling NE release and reuptake further increase the high level of NE at the heart, which will act to enhance the deleterious effects of increased CSNA in HF. NEW & NOTEWORTHY This is the first study, to our knowledge, to compare direct recordings of cardiac sympathetic nerve activity with simultaneously measured cardiac norepinephrine (NE) spillover. Our results indicate that in heart failure, increased cardiac sympathetic nerve activity is a major contributor to the increased NE spillover. In addition, there is enhanced NE spillover for the levels of synaptic nerve activity.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00069.2018
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2018
    detail.hit.zdb_id: 1477308-9
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  • 6
    Online Resource
    Online Resource
    Activation of the carotid body increases directly recorded cardiac sympathetic nerve activity and coronary blood flow in conscious sheep
    American Physiological Society ; 2021
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 320, No. 3 ( 2021-03-01), p. R203-R212
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 320, No. 3 ( 2021-03-01), p. R203-R212
    Abstract: Activation of the carotid body (CB) using intracarotid potassium cyanide (KCN) injection increases coronary blood flow (CoBF). This increase in CoBF is considered to be mediated by co-activation of both the sympathetic and parasympathetic nerves to the heart. However, whether cardiac sympathetic nerve activity (cardiac SNA) actually increases during CB activation has not been determined previously. We hypothesized that activation of the CB would increase directly recorded cardiac SNA, which would cause coronary vasodilatation. Experiments were conducted in conscious sheep implanted with electrodes to record cardiac SNA and diaphragmatic electromyography (dEMG), flow probes to record CoBF and cardiac output, and a catheter to record arterial pressure. Intracarotid KCN injection was used to activate the CB. To eliminate the contribution of metabolic demand on coronary flow, the heart was paced at a constant rate during CB chemoreflex stimulation. Intracarotid KCN injection resulted in a significant increase in directly recorded cardiac SNA frequency (from 24 ± 2 to 40 ± 4 bursts/min; P 〈 0.05) as well as a dose-dependent increase in mean arterial pressure (79 ± 15 to 88 ± 14 mmHg; P 〈 0.01) and CoBF (75 ± 37 vs. 86 ± 42 mL/min; P 〈 0.05). The increase in CoBF and coronary vascular conductance to intracarotid KCN injection was abolished after propranolol infusion, suggesting that the increased cardiac SNA mediates coronary vasodilatation. The pressor response to activation of the CB was abolished by pretreatment with intravenous atropine, but there was no change in the coronary flow response. Our results indicate that CB activation increases directly recorded cardiac SNA, which mediates vasodilatation of the coronary vasculature.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00246.2020
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2021
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  • 7
    Online Resource
    Online Resource
    Hypertonic sodium resuscitation after hemorrhage improves hemodynamic function by stimulating cardiac, but not renal, sympathetic nerve activity
    American Physiological Society ; 2011
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 300, No. 2 ( 2011-02), p. H685-H692
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 300, No. 2 ( 2011-02), p. H685-H692
    Abstract: Small volume hypertonic saline resuscitation can be beneficial for treating hemorrhagic shock, but the mechanism remains poorly defined. We investigated the effects of hemorrhagic resuscitation with hypertonic saline on cardiac (CSNA) and renal sympathetic nerve activity (RSNA) and the resulting cardiovascular consequences. Studies were performed on conscious sheep instrumented with cardiac ( n = 7) and renal ( n = 6) sympathetic nerve recording electrodes and a pulmonary artery flow probe. Hemorrhage (20 ml/kg over 20 min) caused hypotension and tachycardia followed by bradycardia, reduced cardiac output, and abolition of CSNA and RSNA. Resuscitation with intravenous hypertonic saline (1.2 mol/l at 2 ml/kg) caused rapid, dramatic increases in mean arterial pressure, heart rate, and CSNA, but had no effect on RSNA. In contrast, isotonic saline resuscitation (12 ml/kg) had a much delayed and smaller effect on CSNA, less effect on mean arterial pressure, no effect on heart rate, but stimulated RSNA, although the plasma volume expansion was similar. Intracarotid infusion of hypertonic saline (1 ml/min bilaterally, n = 5) caused similar changes to intravenous administration, indicating a cerebral component to the effects of hypertonic saline. In further experiments, contractility (maximum change in pressure over time), heart rate, and cardiac output increased significantly more with intravenous hypertonic saline (2 ml/kg) than with Gelofusine (6 ml/kg) after hemorrhage; the effects of hypertonic saline were attenuated by the β-receptor antagonist propranolol ( n = 6). These results demonstrate a novel neural mechanism for the effects of hypertonic saline resuscitation, comprising cerebral stimulation of CSNA by sodium chloride to improve cardiac output by increasing cardiac contractility and rate and inhibition of RSNA.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00930.2010
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2011
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  • 8
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    Baroreflex mechanisms regulating mean level of SNA differ from those regulating the timing and entrainment of the sympathetic discharges in rabbits
    American Physiological Society ; 2006
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 291, No. 2 ( 2006-08), p. R400-R409
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 291, No. 2 ( 2006-08), p. R400-R409
    Abstract: The arterial baroreflex pathway provides the fundamental basis for the short-term control of blood pressure via the rapid regulation of the mean level of sympathetic nerve activity (SNA) in response to changes in blood pressure. A central tenet in the generation and regulation of bursts of SNA is that input from the arterial baroreceptors also regulates the timing of the bursts of sympathetic activity. With the use of an implantable telemetry-based amplifier, renal SNA was recorded in intact and arterial baroreceptor-denervated (SAD) conscious rabbits. Data were collected continuously while animals were in their home cage. Mean levels of SNA were not different between SAD and baroreceptor-intact animals. Whereas SNA was unresponsive to changes in blood pressure in SAD rabbits, the timing of the bursts of SNA relative to the arterial pulse wave was maintained (time between the diastolic pressure and the next maximum SNA voltage averaged 107 ± 12 ms SAD vs. 105 ± 7 ms intact). Transfer function analysis between blood pressure and SNA indicates the average gain at the heart rate frequency was not altered by SAD, indicating strong coupling between the cardiac cycle and SNA bursts in SAD animals. Further experiments in anesthetized rabbits showed that this entrainment is lost immediately after performing baroreceptor denervation surgery and remained absent while the animal was under anesthesia but returned within 20 min of turning off the anesthesia. We propose that this finding indicates the regulation of the mean level of SNA requires the majority of input from baroreceptors to be functional; however, the regulation of the timing of the bursts in the conscious animal requires only minimal input, such as a sensitive trigger mechanism. This observation has important implications for understanding the origin and regulation of SNA.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00204.2005
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1477297-8
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  • 9
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    Evidence of differential control of renal and lumbar sympathetic nerve activity in conscious rabbits
    American Physiological Society ; 2006
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 290, No. 3 ( 2006-03), p. R701-R708
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 290, No. 3 ( 2006-03), p. R701-R708
    Abstract: We have explored the possibility that renal sympathetic nerve activity (RSNA) and vasomotor sympathetic nerve activity are differentially regulated. We measured sympathetic nerve activity (SNA) to the kidney and the hind limb vasculature in seven conscious rabbits 6–8 days after the implantation of recording electrodes. Acute infusion of N G -nitro-l-arginine methyl ester (l-NAME) (6 mg·kg −1 ·min −1 for 5 min) led to an increase in blood pressure (from 66 ± 1 to 82 ± 3 mmHg) and a decrease in heart rate (from 214 ± 15 to 160 ± 13 bpm). l-NAME administration caused a significantly greater decrease in RSNA than lumbar sympathetic nerve activity (LSNA) (to 68 ± 14% vs. 84 ± 4% of control values, respectively). Volume expansion (1.5 ml·kg −1 ·min −1 ) resulted in a significant decrease in RSNA to 66 ± 7% of control levels but no change in LSNA (127 ± 20%). There was no difference in the gain of the baroreflex curves between the LSNA and RSNA [maximum gain of −7.6 ± 0.4 normalized units (nu)/mmHg for LSNA vs. −7.9 ± 0.75 nu/mmHg for RSNA]. A hypoxic stimulus (10% O 2 and 3% CO 2 ) led to identical increases in both RSNA and LSNA (195 ± 40% and 158 ± 21% of control values, respectively). Our results indicate tailored differential control of RSNA and LSNA in response to acute stimuli.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00504.2005
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1477297-8
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  • 10
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    Septic shock induces distinct changes in sympathetic nerve activity to the heart and kidney in conscious sheep
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 297, No. 5 ( 2009-11), p. R1247-R1253
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 297, No. 5 ( 2009-11), p. R1247-R1253
    Abstract: Sepsis and septic shock are the chief cause of death in intensive care units, with mortality rates between 30 and 70%. In a large animal model of septic shock, we have demonstrated hypotension, increased cardiac output, and tachycardia, together with renal vasodilatation and renal failure. The changes in cardiac sympathetic nerve activity (CSNA) that may contribute to the tachycardia have not been investigated, and the changes in renal SNA (RSNA) that may mediate the changes in renal blood flow and function are unclear. We therefore recorded CSNA and RSNA during septic shock in conscious sheep. Septic shock was induced by administration of Escherichia coli, which caused a delayed hypotension and an immediate, biphasic increase in heart rate (HR) associated with similar changes in CSNA. After E. coli, RSNA decreased for over 3 h, followed by a sustained increase (180%), whereas renal blood flow progressively increased and remained elevated. There was an initial diuresis, followed by oliguria and decreased creatinine clearance. There were differential changes in the range of the arterial baroreflex curves; it was depressed for HR, increased for CSNA, and unchanged for RSNA. Our findings, recording CSNA for the first time in septic shock, suggest that the increase in SNA to the heart is not driven solely by unloading of baroreceptors and that the increase has an important role to increase HR and cardiac output. There was little correlation between the changes in RSNA and renal blood flow, suggesting that the renal vasodilatation was mediated mainly by other mechanisms.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00437.2009
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477297-8
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