Brain angiotensin II and baroreceptor reflex function in spontaneously hypertensive rats.

Cheng, Shan; Kirk, Katharine A.; Robertson, J. D.; Berecek, Kathleen H.

doi:10.1161/01.hyp.14.3.274

Cited by 17 publications

(12 citation statements)

References 37 publications

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“…The site where Ang II affects the baroreflex could include the baroreceptors 26 -27 and the CNS."' 23 However, we found in the present study that enalapril, which suppresses the RAS, exerted no effect on the baroreceptor activity in WKY rats while trichlormethiazide, which may stimulate or at least does not inhibit the RAS, and enalapril had similar effects on the baroreceptor activity in SHRs. It seems unlikely therefore that the anesthesia affected the baroreceptors through actions on the RAS.…”

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confidence: 71%

Effects of antihypertensive agents on baroreceptor function in early hypertensive rats.

et al. 1994

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To investigate the effects of antihypertensive treatment with four currently used agents (trichlormethiazide, atenolol, nicardipine, and enalapril) on the arterial baroreceptor function at the early phase of hypertension, we administered the agents to spontaneously hypertensive rats and WistarKyoto rats from 8 to 10 weeks of age and examined the aortic nerve activity function. In untreated spontaneously hypertensive rats, the relation between the arterial pressure and aortic nerve activity was shifted to the right, that is, to a higher pressure level (threshold pressure, 90±3 versus 76±1 mm Hg, P<.05), and the maximum gain which was obtained by logistic function analysis was depressed (1.55±0.08% versus 2.18±0.13% maximum/mm Hg, f<.01) as compared with untreated Wistar-Kyoto rats. An equivalent decrease in arterial pressure with each of the four agents (-20±l mm Hg, P<.01) B aroreceptor activity transmitted to the central nervous system (CNS) is a primary signal concerning moment-to-moment alterations in arterial pressure and represents a fundamental mechanism in the neural control of the circulation because it triggers reflex inhibition of sympathetic nerve activity and excitation of parasympathetic nerve activity that buffers the rise in pressure. It is known that the baroreceptor function is depressed in several forms of hypertension. 1 " 3 Impaired baroreceptor input to the CNS elicits instability of the circulation, 4 which tends in turn to lead to increases in cardiovascular morbidity and mortality. Agents that effectively potentiate the baroreceptor function are considered preferable in the treatment of hypertension. Early studies have shown that conventional antihypertensive therapy with combinations of drugs (diuretics, vasodilators, and adrenergic antagonists) increased the baroreceptor sensitivity in spontaneously hypertensive rats (SHRs). classes of antihypertensive agents might exert distinct effects on the baroreceptor function through specific pharmacological actions when administered chronically to hypertensive subjects. To test this hypothesis, we treated SHRs with one of four currently used agents (a diuretic, a j3-adrenergic blocker, a calcium channel blocker, and an ACE inhibitor) for 2 weeks and examined the effects on the aortic baroreceptor function. Moreover, we used relatively young SHRs (10 weeks of age) in which the characteristics of the aorta are less damaged by hypertension 3

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confidence: 71%

Effects of antihypertensive agents on baroreceptor function in early hypertensive rats.

et al. 1994

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“…These data suggest that ACE inhibitors, more than antirenin immunization, reduce the generation of angiotensin II within the central nervous system, where it specifically depresses cardiac baroreceptor reflex responses to increases, but not to decreases, in blood pressure. 27 - 28 However, it has been recently shown that brain ACE was not consistently decreased by most of the ACE inhibitors. 29 In addition, antirenin immunization also tended to increase the baroreceptor reflex sensitivity.…”

Section: Figure 4 Bar Graphs Showing the Free Urinary Catecholaminesmentioning

confidence: 99%

Antirenin immunization versus angiotensin converting enzyme inhibition in rats.

Julien

Michel

et al. 1990

Hypertension

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The effects of specific active immunization against renin were compared with those of chronic angiotensin converting enzyme (ACE) inhibition. Male spontaneously hypertensive rats (SHR) were immunized (SHR-I) (n=10) against pure murine renin (four injections of 30 /ig/kg s.c) or received (SHR-P) (n=ll) a converting enzyme inhibitor (perindopril, 2 mg/kg/day per os for 4 weeks). Sham-immunized SHR (SHR-S) (n=12) and normotensive Wistar-Kyoto (WKY-S) (n=12) rats served as controls. At 15 weeks of age, 24-hour average blood pressure was obtained in freely moving rats using intra-aortic pressure recording with computer analysis. Antirenin immunization induced high circulating titers of antibodies, a fall in plasma renin activity (-95%), and urinary excretion of mineralocorticoids. Perindopril abolished the pressor response to angiotensin I, whereas plasma ACE was only partly (-56%) decreased. It also increased plasma renin activity and did not alter the urinary excretion of steroids. Both immunization and perindopril allowed the blood pressure of SHR to return to the level of WKY-S rats and reduced the left ventricular weight These decreases were associated with an elevated sympathetic nervous system activity as indicated by increases in the urinary excretion of catecholamines and their metabolites. It is concluded that, apart from an unaltered steroid synthesis, most of the cardiovascular effects of chronic ACE inhibition are similar to those of antirenin immunization, thus indicating that blockade of the circulating and renal reninangiotensin system accounts for most of the effects of ACE inhibitors. (Hypertension 1990; 16:80-88)

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“…Berecek and colleagues (15)(16)(17)(18)(19)(20)(21) have shown that lifelong treatment of SHR by an angiotensin-converting enzyme inhibitor, captopril, completely blocks the development of hypertension and related cardiovascular derangements in adult animals. Even when treatment is discontinued at age 8 wk, captopril-treated SHR (cap-SHR) indefinitely maintain normal blood pressure and heart rate (15)(16)(17)(18)(19)(20)(21), as well as an absence of the vascular changes and cardiac hypertrophy typically observed in SHR (19).…”

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Sleep-disordered Respiration in Phenotypically Normotensive, Genetically Hypertensive Rats

Carley

Berecek

Videnović

et al. 2000

Am J Respir Crit Care Med

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Increased prevalence of sleep-related breathing disorders has been reported in patients with essential hypertension and we have described disordered breathing in spontaneously hypertensive rats, an animal model of genetic hypertension. The mechanisms coupling hypertension to respiratory dysfunction during sleep remain, however, largely unknown. To determine if sleep-related respiratory disorder reflects cardiovascular derangement or, alternatively, represents an independent phenotype in hypertensive rats, we polygraphically recorded groups (n = 10) of genetically hypertensive, genetically normotensive, and phenotypically normotensive rats carrying a genetic background for hypertension. Apnea index was elevated more than 15-fold during NREM sleep in both animal groups carrying hypertension-related genes (p < 0.0001 for each) versus normotensive Wistar Kyoto rats. During REM sleep, a genetic background for hypertension was associated with an increased apnea index of at least 500% versus normotensive Wistar Kyoto rats (p < 0.0001 for each comparison). Still, overall mean respiratory rate, minute ventilation, and sleep architecture were equivalent among all animal groups. As expected, blood pressure and heart period were similar in both normotensive groups but elevated in the hypertensive animals. Persistent sleep-related breathing disorder despite effective cardiovascular normalization in the phenotypically normotensive but genetically hypertensive rats suggests that disordered breathing represents a genetically determined phenotype in these animals that is not secondary to the cardiovascular derangements. The model system described here may provide a powerful tool for investigation of the determinants of sleep-related breathing disorder.

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Brain angiotensin II and baroreceptor reflex function in spontaneously hypertensive rats.

Cited by 17 publications

References 37 publications

Effects of antihypertensive agents on baroreceptor function in early hypertensive rats.

Effects of antihypertensive agents on baroreceptor function in early hypertensive rats.

Antirenin immunization versus angiotensin converting enzyme inhibition in rats.

Sleep-disordered Respiration in Phenotypically Normotensive, Genetically Hypertensive Rats

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