Angiotensin II exerts differential actions on renal nerve activity and heart rate.

Kumagai, Kazuhiro; Reid, Ian A.

doi:10.1161/01.hyp.24.4.451

Cited by 44 publications

(52 citation statements)

References 33 publications

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“…In dogs, rabbits, and rats, systemic administration of ANG II has been demonstrated to increase blood pressure without causing the large reflex bradycardia that normally accompanies such increases in blood pressure suggesting that ANG II resets the baroreflex control of HR to a higher pressure (29,39). It is widely accepted that this effect of ANG II is due to central actions of this peptide on circumventricular organs such as area postrema (30,34).…”

Section: Discussionmentioning

confidence: 99%

“…In addition to its peripheral vasoconstrictor effects, this peptide has been known to modulate reflex regulation of HR and sympathetic activity through circumventricular organs such as the area postrema (13, 37). In rabbits, dogs, and rats, acute increases in circulating ANG II blunt baroreflex regulation of HR (1,31,38,39). It is interesting to know if centrally mediated effects of ANG II on baroreflex function are affected by differences in circulating estrogen levels and gender.…”

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confidence: 99%

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Estrogen modulation of baroreflex function in conscious mice

Pamidimukkala

Taylor

Welshons

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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.-It has been suggested that estrogen modulates baroreflex regulation of autonomic function. The present study evaluated the effects of estrogen on baroreflex regulation of heart rate in response to changes in blood pressure with phenylephrine (PE), ANG II, and sodium nitroprusside (SNP) in a conscious mouse model. Males and ovariectomized females with (OvxEϩ) and without (OvxEϪ) estradiol replacement chronically implanted with arterial and venous catheters were used in these studies. The slope of the baroreflex bradycardic responses to PE was significantly facilitated in OvxEϩ females (Ϫ7.65 Ϯ 1.37) compared with OvxEϪ females (Ϫ4.5 Ϯ 0.4). Likewise, the slope of the baroreflex bradycardic responses to ANG II was significantly facilitated in OvxEϩ females (Ϫ7.97 Ϯ 1.06) compared with OvxEϪ females (Ϫ4.8 Ϯ 1.6). Reflex tachycardic responses to SNP were comparable in all the groups. Finally, in male mice, the slope of ANG II-induced baroreflex bradycardia (Ϫ5.17 Ϯ 0.95) was significantly less than that induced by PE (Ϫ8.50 Ϯ 0.92), but this ANG II-mediated attenuation of reflex bradycardia was not observed in the female mice. These data support the hypothesis that estrogen facilitates baroreflex function in female mice and suggest that ANG II-mediated acute blunting of baroreflex regulation of heart rate may be sex dependent. gender differences; autonomic regulation; cardiac baroreflexes EPIDEMIOLOGICAL STUDIES have shown that cardiovascular diseases such as hypertension and coronary heart disease are less common in premenopausal women compared with age-matched men (16,18,23,50). This innate protection in women against cardiovascular disease disappears with reproductive senescence or with removal of endogenous ovarian steroids (4,45,49).It is thought that estrogen may affect cardiovascular function at numerous levels including the vasculature, heart, and brain (36, 46). A potential mechanism by which estrogen provides cardioprotection in women is by acting at central cardiovascular regulatory centers to modulate autonomic regulation of the cardiovascular system. Hormone replacement therapy appears to have favorable effects on the cardiovascular autonomic regulation in postmenopausal women by improving baroreflex sensitivity and overall heart rate (HR) variability (19). Similar observations have also been made in male and ovariectomized female rats where estrogen replacement appears to improve baroreflex sensitivity via central mechanisms (32,43). However, to date, there have been no studies about the role of estrogen or gender in baroreflex control of HR in mice.ANG II is a potent circulatory peptide implicated in pathogenesis of hypertension. In addition to its peripheral vasoconstrictor effects, this peptide has been known to modulate reflex regulation of HR and sympathetic activity through circumventricular organs such as the area postrema (13, 37). In rabbits, dogs, and rats, acute increases in circulating ANG II blunt baroreflex regulation of HR (1,31,38,39). It is interesting to know if centrally mediated e...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Estrogen modulation of baroreflex function in conscious mice

Pamidimukkala

Taylor

Welshons

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…9,23 In conscious rabbits, Kumagai and Reid 9 found that both an ACE inhibitor and an angiotensin type I receptor antagonist decreased arterial pressure and increased renal sympathetic nerve activity, whereas heart rate was unchanged. Thus, Ang II resets the baroreflex control of heart rate, leaving the control of renal nerve activity unaffected.…”

Section: Discussionmentioning

confidence: 99%

“…7,8 The aim of the present study was to assess the effect of short-term ACE inhibition on the adrenergic drive in patients with hypertension and renal artery stenosis. Given that animal experiments indicate different effects on renal nerve activity and heart rate in response to Ang II, 9 we also wanted to explore whether there is regional differentiation in the sympathetic response to ACE inhibition and nonspecific vasodilatation, with the latter used as a positive control test.…”

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confidence: 99%

Differentiated Response of the Sympathetic Nervous System to Angiotensin-Converting Enzyme Inhibition in Hypertension

et al. 2000

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Abstract-Hypertension with renal artery stenosis is associated with both an activated renin-angiotensin system and elevated sympathetic activity. Therefore, in this condition it may be favorable to use a therapeutic modality that does not reflexly increase heart rate, renin secretion, and sympathetic nervous activity. The purpose of the present study was to assess overall, renal, and muscle sympathetic activity after short-term administration of an angiotensin-converting enzyme inhibitor (enalaprilat) and a nonspecific vasodilator (dihydralazine) to hypertensive patients with renal artery stenosis. Forty-eight patients undergoing a clinical investigation for renovascular hypertension were included in the study. An isotope dilution technique for assessing norepinephrine spillover was used to estimate overall and bilateral renal sympathetic nerve activity. In 11 patients simultaneous intraneural recordings of efferent muscle sympathetic nerve activity were performed. Thirty minutes after dihydralazine administration, mean arterial pressure fell by 15%, whereas plasma angiotensin II, muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover increased (PϽ0.05 for all). In contrast, after enalaprilat administration a fall in arterial pressure similar to that for dihydralazine was followed by decreased angiotensin II levels and unchanged muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover, whereas renal norepinephrine spillover increased by 44% (PϽ0.05). Acute blood pressure reduction by an angiotensin-converting enzyme inhibitor provokes a differentiated sympathetic response in patients with hypertension and renal artery stenosis, inasmuch that overall and muscle sympathetic reflex activation are blunted, whereas the reflex renal sympathetic response to blood pressure reduction is preserved. (Hypertension. 2000;36:543-548.)Key Words: hypertension, renovascular Ⅲ sympathetic nervous system Ⅲ renin-angiotensin system R enovascular hypertension is a condition associated with both an activated renin-angiotensin system and elevated sympathetic nerve activity. 1,2 Previous data, obtained in experimental models, indicate a positive interaction between the renin-angiotensin and the sympathetic nervous systems. 3 Therefore, in renovascular hypertension it may be favorable to use a therapeutic modality that does not reflexly further increase heart rate, renin secretion, and sympathetic nervous activity. It is well known that certain drugs used in cardiovascular medicine affect various indices of sympathetic activity. For example, sympathetic activity increases in response to nonspecific vasodilators, whereas therapy with angiotensin-converting enzyme (ACE) inhibitors has demonstrated reduced peroneal sympathetic activity. 4 Thus, it appears that vasodilators and ACE inhibitors produce different sympathetic nerve responses; the effects of the latter could be due to either a direct-acting central mechanism 5,6 or a reduction of angiotensin II (Ang II) facilitatory e...

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“…Angiotensin II diminishes the sensitivity of this reflex by synaptically inhibiting it in the nucleus tractus solitarii, by increasing sympathetic nerve activity while decreasing the vagal tone to the heart. It also directly stimulates the myocardium, thus, shifting the operating 'set-point' for regulation of sympathetic outflow to higher BP (Isaacson & Reid, 1990;Kumagai & Reid, 1994;Averill, 2000;Averill & Diz, 2000;Bader et al, 2001;Balt et al, 2003;Diz et al, 2008;Smith et al, 2008;Hilzendeger et al, 2010;Arnold et al, 2011). This may explain the reductions in HR observed with the two highest doses of ang II given alone (figure 4.15).…”

Section: Does T Violacea Act By Blocking the Angiotensin II Receptors?mentioning

confidence: 98%

Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats

Raji

Mugabo

Obikeze

2012

Journal of Ethnopharmacology

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Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats I. A. RAJITulbaghia violacea Harv. (Alliaceae) is a small bulbous herb which belongs to the family, Alliaceae, most commonly associated with onions and garlic. In South Africa (SA), this herb has been traditionally used in the treatment of various ailments, including fever, colds, asthma, paralysis, hypertension (HTN) and stomach problems. The aim of this study was to evaluate the effect of methanol leaf extracts (MLE) of T. violacea on the blood pressure (BP) and heart rate (HR) in anaesthetized male spontaneously hypertensive rats; and to find out the mechanism(s) by which it acts.The MLE of T. violacea (5 -150 mg/kg), angiotensin I (ang I, 3.1 -100 µg/kg), captopril (10 mg/kg), angiotensin II (ang II, 3.1 -50 µg/kg), losartan (30 mg/kg), phenylephrine T. violacea (60 mg/kg) and captopril (10 mg/kg) were injected intraperitoneally into iii some SHR for 21 days to investigate the chronic effect of these agents on plasma levels of aldosterone. The mean change, the mean of the individual percentage changes and the percentage difference (in mean) observed with each intervention was calculated and statistically analyzed using the Student's t test for significant difference (p < 0.05). The Microsoft Excel software was used for statistical analysis.T. violacea significantly (p < 0.05) reduced the systolic, diastolic, and mean arterial BP;and HR dose-dependently. In a dose-dependent manner, ang I, ang II, phenylephrine significantly (p < 0.05) increased the BP, while propranolol, muscarine and atropine reduced the BP. The increases in BP due to dobutamine were not dose-dependent. In a dose dependent manner, phenylephrine and propranolol reduced the HR, while dobutamine increased the HR. The effect of ang I, ang II, muscarine and atropine on HR were not dose-dependent; with both increases as well as decreases observed with ang I, and II and atropine, while decreases were seen with muscarine. Captopril produced significant (p < 0.05) reduction in BP which were not associated with any change in HR.The co-infusion of ang I with the MLE produced significant (p < 0.05) reduction in BP, which were not associated with significant changes in HR. The co-infusion of ang II with the MLE did not produce any significant changes in BP or HR when compared to the infusion of the standard drug alone. The co-infusion of phenylephrine with the MLE did

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Angiotensin II exerts differential actions on renal nerve activity and heart rate.

Cited by 44 publications

References 33 publications

Estrogen modulation of baroreflex function in conscious mice

Estrogen modulation of baroreflex function in conscious mice

Differentiated Response of the Sympathetic Nervous System to Angiotensin-Converting Enzyme Inhibition in Hypertension

Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats

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