The brain renin‐angiotensin system

Severs, Walter B.; Summy-Long, Joan Y.; Keil, L. C.

doi:10.1002/ddr.430020303

Cited by 12 publications

(6 citation statements)

References 51 publications

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“…Centrally administered Ang II also increases blood pressure and this effect is especially important in hypovolemic conditions (12,15,16,19,(29)(30)(31). Intracerebroventricular injections of renin-angiotensin system antagonists decrease blood pressure in spontaneously hypertensive and normotensive rats (9,17,19,20,32,33).…”

Section: Discussionmentioning

confidence: 99%

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Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline

Isbil-Buyukcoskun

Gulec

Ozluk

et al. 2001

Braz J Med Biol Res

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In the present study, we investigated the involvement of the brain renin-angiotensin system in the effects of central cholinergic stimulation on blood pressure in conscious, freely moving normotensive rats. In the first step, we determined the effects of intracerebroventricular (icv) choline (50, 100 and 150 µg) on blood pressure. Choline increased blood pressure in a dose-dependent manner. In order to investigate the effects of brain renin-angiotensin system blockade on blood pressure increase induced by choline (150 µg, icv), an angiotensin-converting enzyme inhibitor, captopril (25 and 50 µg, icv), was administered 3 min before choline. Twenty-five µg captopril did not block the pressor effect of choline, while 50 µg captopril blocked it significantly. Our results suggest that the central renin-angiotensin system may participate in the increase in blood pressure induced by icv choline in normotensive rats. CorrespondenceN.

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Section: Discussionmentioning

confidence: 99%

“…All elements of the renin-angiotensin system have been identified in brain tissue (12)(13)(14)(15). Central angiotensin II (Ang II) increases arterial blood pressure, stimulates drinking behavior, increases VP and corticotropin secretion and inhibits renin secretion (12,(16)(17)(18)(19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline

Isbil-Buyukcoskun

Gulec

Ozluk

et al. 2001

Braz J Med Biol Res

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“…However, there is strong evidence that the brain is capable of independently generating All via an endogenous brain enzymatic system. 21 Furthermore, it has been hypothesized that the brain renin-angiotensin system is activated by relative sodium retention, 22 such as occurs in one-kidney, one clip renal hypertension. It is possible, then, that renal artery constriction activates neurohormonal pressor systems emanating from, or passing through, the AV3V region by mediation of endogenously generated All within the brain.…”

Section: Discussionmentioning

confidence: 99%

Forebrain contributions to one-kidney renal hypertension in the rabbit.

Fink

Mann²

1983

Hypertension

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SUMMARY Electrolytic lesions were placed along the anteroventral wall of the third cerebral ventricle (AV3V region) in 10 albino rabbits (AV3V-X), and sham lesions were produced in 10 additional rabbits (SHAM). Two to 3 weeks later, all rabbits underwent unilateral nephrectomy and renal artery stenosis (clip I.D. = 0.508 mm). During a 1-week control period, and for 4 weeks after renal artery stenosis, measurements were made of mean arterial pressure (MAP), heart rate, body fluid compartment volumes, plasma electrolytes, and dairy sodium, potassium, and water balances. Four weeks after renal artery stenosis (RAS), cardiovascular responses to norepinephrine (NE), angiotensin II (All), saralasin, and autonomic blockade were obtained in the conscious animals. In SHAM rabbits, MAP rose from 77 to 117 mm Hg 4 weeks after RAS. In AV3V-X rabbits, MAP rose from 77 to only 92 mm Hg 4 weeks after RAS. Body fluid compartment volumes, plasma electrolytes, and fluid, sodium, and potassium balances showed similar modest changes in both groups of rabbits. Neither saralasin infusion nor autonomic blockade caused significantly different changes in MAP between SHAM and AV3V-X rabbits 4 weeks after RAS. However, pressor responses to both NE and All were significantly less in AV3V-X rabbits at this time. It is concluded that one-kidney, one clip renal hypertension involves activation of neurohormonal pressor mechanisms originating in the forebrain, and that the expression of these pressor mechanisms in part includes an increase in cardiovascular reactivity. nervous system mechanisms controlling arterial blood pressure make a critical contribution to the development and maintenance of experimental renal hypertension. An important part of this evidence is the demonstration that disruption of various brain regions involved in cardiovascular regulation, either with electrolytic lesions' or neurotoxins, 2 prevents or retards the development of experimental renal hypertension in several different animal models. Recent studies of this type in the rat have centered upon brain structures of the anteroventral wall of the third cerebral ventricle (AV3V), a forebrain area known to contain neuronal elements sensitive to blood and cerebral fluid osmolality, and All concentration. Although the known ability of AV3V lesions in the rat to reduce or abolish many physiological responses to All and osmotic stimulation suggest an appealing link between renal manipulations and abnormal neural cardiovascular control in renal hypertension, 1 a somewhat atypical distribution of All-sensitive neurons in the rat brain 7 raises the question of the applicability to other species of conclusions obtained in experiments on rats alone. Thus, we have undertaken an examination of the influence of AV3V lesions on renal hypertension development in another common experimental animal -the rabbit. In a prior report, we showed that AV3V lesions in the rabbit did not alter the pathogenesis of two-kidney, one clip renal hypertension. 8 In the current study, we assessed the e...

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“…A cannula [17] was implanted into the left lateral cerebroventricle under pentobarbital sodium anesthesia (45 mg/kg i.p.). A minimum of 3 days was allowed for recovery.…”

Section: Methodsmentioning

confidence: 99%

Vasopressin Release Induced by Water Deprivation: Effects of Centrally Administered Saralasin

et al. 1983

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Uncertainty exists as to whether endogenous angiotensin activates brain mechanisms controlling vasopressin (AVP) secretion during dehydration. We injected various doses of saralasin into a lateral cerebroventricle (IVT) of conscious, male rats deprived of water for 48 h and killed them at different times. The concentration of AVP in the plasma (p[AVP]), measured by radioimmunoassay, was unaffected by saralasin. IVT pretreatment with 1-Sar-8-Ile-angiotensin II blocked maximal AVP release by IVT angiotensin, but this pretreatment did not reduce p[AVP] after 24, 48 or 72 h water deprivation. A 3-hour continuous IVT infusion of CSF or saralasin (10 μg/h) into 48-hour water-deprived rats revealed equivalent p[AVP] and urine volumes. When the infusions were continued for 3 h more with water available, control and saralasin-treated rats: (a) drank at similar rates, (b) excreted similar amounts of urine, and (c) reduced their p[AVP] levels to the same extent. IVT saralasin did not affect p[AVP] of rats dehydrated with hypertonic NaCl. Combined IVT saralasin and atropine reduced p[AVP] of 48-hour water deprived rats about 30% (p < 0.05). We conclude that redundancy exists for sensing, integrating and releasing vasopressin in dehydrated rats.

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The brain renin‐angiotensin system

Cited by 12 publications

References 51 publications

Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline

Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline

Forebrain contributions to one-kidney renal hypertension in the rabbit.

Vasopressin Release Induced by Water Deprivation: Effects of Centrally Administered Saralasin

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