Nitric oxide modulates arterial baroreflex control of heart rate in conscious lambs in an age-dependent manner

2001 ◽  
Vol 280 (5) ◽  
pp. H2255-H2263 ◽  
Author(s):  
Alp Sener ◽  
Francine G. Smith
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Intravenous Administration ◽  
Systolic Arterial Pressure ◽  
Dependent Manner ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Postnatal Maturation ◽  
Age Dependent ◽  
Before And After

Experiments were carried out in conscious chronically instrumented lambs aged 1 ( n = 6) and 6 wk ( n = 5) to evaluate the arterial baroreflex control of heart rate (HR) during postnatal maturation and to investigate any modulatory role of endogenously produced nitric oxide (NO). Before and after intravenous administration of 20 mg/kg of the l-arginine analog N G-nitro-l-arginine methyl ester (l-NAME), the arterial baroreflex was assessed by measuring HR responses to increases and decreases in systolic arterial pressure achieved by intravenous administration of phenylephrine and sodium nitroprusside. The HR range over which the baroreflex operates and minimum HR as well as maximum gain were greater at 1 than at 6 wk of age. These age differences were abolished in the presence ofl-NAME, which decreased the HR range and gain of the arterial baroreflex control of HR at 1 but not at 6 wk of age. These data provide new information that age-dependent effects of the arterial baroreflex appear to result from effects of endogenously produced NO.

scholarly journals Nitric oxide and angiotensin II regulate cardiovascular homeostasis and the arterial baroreflex control of heart rate in conscious lambs

2011 ◽  
Vol 13 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Stephanie J Wehlage ◽  
Francine G Smith
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Before And After ◽  
Cardiovascular Homeostasis ◽  
New Evidence

To investigate the potential role of angiotensin II (Ang II) type 1 receptors (AT1Rs) as well as endogenously produced nitric oxide (NO) in regulating cardiovascular homeostasis during ontogeny, experiments were carried out in conscious lambs aged approximately 1 week ( N = 9) and 6 weeks ( N = 11). The arterial baroreflex control of heart rate (HR) was assessed before and after intravenous (IV) infusion of the selective AT1R antagonist, ZD 7155, before and after IV administration of the L-arginine analogue, NG-nitro-L-arginine methyl ester (L-NAME). In both groups, after ZD 7155 alone, mean arterial pressure decreased then increased after L-NAME. At 1 but not 6 weeks, HR decreased after ZD 7155 as well as after L-NAME. At 1 but not 6 weeks, there was a decrease in the HR range after ZD 7155 and after ZD 7155 + L-NAME, as compared to control. There was also a decrease in minimum HR after ZD 7155 + L-NAME at 1 week. These data provide new evidence that, together, Ang II and NO regulate cardiovascular homeostasis as well as the arterial baroreflex of HR early in life which may help to explain the activation of these two systems early in life.

Kappa opioids modulate the arterial baroreflex control of heart rate in conscious young sheep

2007 ◽  
Vol 85 (8) ◽  
pp. 811-817 ◽  
Author(s):  
Wei Qi ◽  
Francine G. Smith
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Direct Evidence ◽  
Opiate Receptors ◽  
Random Order ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Physiological Conditions ◽  
Kappa Opioids ◽  
Before And After

The present study tested the hypothesis that κ-opioids modulate the arterial baroreflex control of heart rate in conscious young sheep. Various parameters governing the arterial baroreflex control of heart rate were assessed before and after activation of κ-opiate receptors (KOR) by i.v. administration of the specific KOR agonist U-50488H (experiment 1) or vehicle (experiment 2) to conscious, chronically instrumented lambs aged 42 ± 2 days (n = 6). The 2 experiments were administered in random order at minimum intervals of 48 h. Thirty min after U-50488H treatment, there was an increase in diastolic and mean arterial pressure and in heart rate, returning to control levels by 90 min. A significant increase in the arterial pressure at the midpoint of the baroreflex range and in the minimum heart rate as well as a significant decrease in the heart rate range over which the arterial baroreflex operates were also seen at 30 min after U-50488H, gradually returning to control levels over 120 min. Vehicle had no effect on any of the parameters governing the arterial baroreflex control of heart rate. These data provide the first direct evidence that under physiological conditions in young lambs, the arterial baroreflex control of heart rate is altered after administration of the specific KOR agonist U-50488H, revealing a previously unidentified role for this opioid receptor.

scholarly journals Blockade of neuronal nitric oxide synthase alters the baroreflex control of heart rate in the rabbit

1998 ◽  
Vol 274 (1) ◽  
pp. R181-R186 ◽  
Author(s):  
Hiroshi Murakami ◽  
Jun-Li Liu ◽  
Hirohito Yoneyama ◽  
Yasuhiro Nishida ◽  
Kenji Okada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
No Synthase ◽  
Baroreflex Control ◽  
Neuronal No Synthase ◽  
Significant Difference ◽  
Before And After ◽  
Synthase Inhibitor ◽  
Oxide Synthase

In previous studies we used N G-nitro-l-arginine (l-NNA) to investigate the role of nitric oxide (NO) in baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA).l-NNA increased resting mean arterial pressure (MAP), decreased HR, and did not change or slightly decreased RSNA. These changes complicated the assessment of the central effects of NO on the baroreflex control of HR and RSNA. Therefore, in the present study the effects of the relatively selective neuronal NO synthase inhibitor 7-nitroindazole (7-NI) on the baroreflex control of HR and RSNA were investigated in rabbits. Intraperitoneal injection of 7-NI (50 mg/kg) had no effect on resting HR, MAP, or RSNA. 7-NI significantly reduced the lower plateau of the HR-MAP baroreflex curve from 140 ± 4 to 125 ± 4 and from 177 ± 10 to 120 ± 9 beats/min in conscious and anesthetized preparations, respectively ( P < 0.05). In contrast, there was no significant difference in the RSNA-MAP curves before and after 7-NI administration in conscious or anesthetized preparations. These data suggest that blockade of neuronal NO synthase influences baroreflex control of HR but not of RSNA in rabbits.

Age-dependent renal responses to the bradykinin B2- receptor antagonist icatibant in conscious lambs

2001 ◽  
Vol 281 (4) ◽  
pp. R1311-R1318 ◽  
Author(s):  
Avni Patel ◽  
Francine G. Smith
Keyword(s):  
Receptor Antagonist ◽  
Tubular Function ◽  
Urinary Flow ◽  
Dependent Manner ◽  
Postnatal Maturation ◽  
Age Dependent ◽  
Before And After ◽  
Excretion Rates ◽  
Renal Responses

To investigate the role of endogenously produced bradykinin in modulating renal function during postnatal maturation, various parameters of glomerular and tubular function were measured for 1 h before and after intravenous injection of 12.5 μg/kg of the specific B2-receptor antagonist icatibant to conscious, chronically instrumented lambs aged ∼1 ( n = 7) and ∼6 wk ( n = 7). In response to icatibant, and in the absence of any changes in renal hemodynamics, there was an ∼80% decrease in glomerular filtration rate (GFR) at 20 min in 1-wk-old lambs that was sustained for 60 min; in 6-wk-old lambs, there was an ∼70% decrease in GFR by 20 min, with control levels being reached by 40 min. Icatibant administration was also associated with significant decreases in urinary flow, Cl−, and K+ excretion rates that were similar in both groups of lambs, whereas Na+ excretion decreased only in 6-wk-old lambs. We conclude that bradykinin modulates glomerular and tubular function in an age-dependent manner.

alpha-ANP alters reflex control of lumbar and renal sympathetic nerve activity and heart rate

1987 ◽  
Vol 253 (5) ◽  
pp. H1136-H1140 ◽  
Author(s):  
T. Imaizumi ◽  
A. Takeshita ◽  
H. Higashi ◽  
M. Nakamura
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Vagal Afferents ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Arterial Baroreceptors ◽  
Before And After ◽  
Bilateral Vagotomy

This study examined the effects of synthetic alpha-rat atrial natriuretic peptide (alpha-rANP) on arterial pressure (AP), heart rate (HR), and renal and lumbar sympathetic nerve activity (SNA) in rats with intact arterial baroreceptors before and after bilateral vagotomy and in those with sinoaortic denervation before and after vagotomy. In intact rats, alpha-rANP decreased AP, which was accompanied by the decrease in renal SNA ad HR and no change in lumbar SNA. In contrast, the increase in lumbar SNA and HR occurred during hypotension caused by nitroglycerin. In rats with intact arterial baroreceptors and vagi sectioned, renal and lumbar SNA and HR did not change during hypotension with alpha-rANP. In addition, alpha-rANP did not alter the gain of arterial baroreflex control of lumbar SNA in these rats. In rats with sinoaortic denervation, alpha-rANP decreased HR and renal and lumbar SNA before vagotomy but did not change them after vagotomy. These results suggest, first, that alpha-rANP activates vagal afferents and thereby inhibits renal and lumbar SNA and HR and, second, that alpha-rANP may reset arterial baroreflex control of SNA and HR to a lower pressure range.

Effects of coronary occlusion on arterial baroreflex control of heart rate and vascular resistance

1987 ◽  
Vol 252 (4) ◽  
pp. H749-H759 ◽  
Author(s):  
B. Trimarco ◽  
B. Ricciardelli ◽  
A. Cuocolo ◽  
M. Volpe ◽  
N. De Luca ◽  
...  
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Intravenous Administration ◽  
Coronary Occlusion ◽  
Left Ventricular ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Parasympathetic System ◽  
Anesthetized Dogs ◽  
Sympathetic Efferents

This study was planned to assess whether circumflex coronary occlusion (CO) impairs the arterial baroreflex control of heart rate (HR) and hindlimb vascular resistance (HVR), and to determine the mechanisms involved in the mediation of these phenomena. Increasing doses of phenylephrine and nitroglycerin were given intravenously to anesthetized dogs with a constant flow-perfused hindlimb before and during 30-s CO. The reflex responses were assessed by the changes in HR and hindlimb perfusion pressure evoked by changes in arterial pressure following phenylephrine and nitroglycerin administration. During CO, there was an attenuation of the reflex control of HR and HVR as compared with control conditions. The application of lidocaine on the left ventricular epicardial surface was able to prevent the effect of CO on both the baroreflex responses. The intravenous administration of atropine prevented only the impairment in arterial baroreflex control of HR induced by CO. After the injection of phentolamine into the perfused hindlimb, the baroreflex had no effect on HVR either before or during CO. Finally, intravenous administration of propranolol failed to modify the effect of CO on both the baroreflex responses. These data indicate that CO attenuates the arterial baroreflex control of both HR and HVR through the stimulation of left ventricular receptors. The effect on HR is mediated by the parasympathetic system, whereas the effect on HVR is due to sympathetic efferents.

scholarly journals Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vital Role ◽  
Initial Increase ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

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