Effects of intracerebroventricular captopril on angiotensin-converting enzyme and angiotensinogen mRNA levels in rat brain

Ye, Ming-Qi; Yuan, Long-Xing; Healy, Dennis P.

doi:10.1016/0922-4106(92)90145-l

Cited by 3 publications

(3 citation statements)

References 9 publications

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“…When the precursor ANG I or the enzyme renin is intracerebroventricularly injected, the dipsogenic ANG II is produced by the brain, perhaps in the circumventricular organs (33). Inhibition of the intracerebral angiotensin-converting enzyme by means of intracerebroventricular administration of Cap blocks this process and renders the intracerebroventricularly injected ANG I and renin ineffective (7,10,48,49). Hence, our finding that intracerebroventricular Cap suppresses the Oct-induced responses suggests that the intracerebral formation of ANG II is necessary for these effects.…”

Section: Discussionmentioning

confidence: 74%

Octreotide-induced drinking, vasopressin, and pressure responses: role of central angiotensin and ACh

Hajdu

Obál²,

Gardi

et al. 2000

American Journal of Physiology-Regulatory, Integrative and Comp

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The involvement of central angiotensinergic and cholinergic mechanisms in the effects of the intracerebroventricularly injected somatostatin analog octreotide (Oct) on drinking, blood pressure, and vasopressin secretion in the rat was investigated. Intracerebroventricular Oct elicited prompt drinking lasting for 10 min. Water consumption depended on the dose of Oct (0.01, 0.1, and 0. 4 microgram). The drinking response to Oct was inhibited by pretreatments with the intracerebroventricularly injected angiotensin-converting enzyme inhibitor captopril, the AT(1)/AT(2) angiotensin receptor antagonist saralasin, the selective AT(1) receptor antagonist losartan, or the muscarinic cholinergic receptor antagonist atropine. The dipsogenic effect of Oct was not altered by prior subcutaneous injection of naloxone. Oct stimulated vasopressin secretion and enhanced blood pressure. These responses were also blocked by pretreatments with captopril or atropine. Previous reports indicate that the central angiotensinergic and cholinergic mechanisms stimulate drinking and vasopressin secretion independently. We suggest that somatostatin acting on sst2 or sst5 receptors modulates central angiotensinergic and cholinergic mechanisms involved in the regulation of fluid balance.

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Section: Discussionmentioning

confidence: 74%

Octreotide-induced drinking, vasopressin, and pressure responses: role of central angiotensin and ACh

Hajdu

Obál²,

Gardi

et al. 2000

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Although renin is rate limiting in its reaction with angiotensinogen in the bloodstream, in local tissue sites, such as the adrenal (Kim et al 1992), DCPl or angiotensinogen may be the rate limiting components, at least in the SHRSP. In rat brain, captopril, a DCPl inhibitor, suppresses DCPl mRNA (Ye et al 1992). In SHR, enhanced arterial DCP 1 enzyme concentration early in life has been suggested to contribute to the development…”

Section: C P I : a Human Hypertension Locus?mentioning

confidence: 99%

“…In rat brain, captopril, a DCPl inhibitor, suppresses DCPl mRNA (Ye et al 1992). In SHR, enhanced arterial DCP 1 enzyme concentration early in life has been suggested to contribute to the development …”

Section: Introductionmentioning

confidence: 98%

CHROMOSOME 17q23: A LOCUS FOR CARDIOVASCULAR DISEASE

Morris

1993

Clin Exp Pharma Physio

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1. The gene for dipeptidyl carboxypeptidase 1 (angiotensin I-converting enzyme, kininase II; DCP1), located on chromosome 17q23, has been implicated in hypertension in rats. In humans associations have been found for the insertion allele of a bi-allelic insertion/deletion polymorphism of DCP1 with hypertension and the deletion allele with myocardial infarction. Other hypertension studies have, however, failed to find a relationship. 2. Mathematical predictions based on DCP1 association data suggest that high sib-pair numbers may be needed to achieve statistical significance by this approach, although differences in the severity of hypertension in different study groups could account for the disparate findings. 3. No association was found between DCP1 allele or genotype frequencies and obesity in essential hypertensives.

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Angiotensinogen

Tewksbury

2000

Comprehensive Physiology

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The sections in this article are: Primary Structure Kinetics of the Renin‐Angiotensinogen Reaction Regulation Hormonal Regulation Transcriptional and Translational Regulation In Vivo Manipulation of Angiotensinogen Gene Expression Tissue Renin–Angiotensin Systems Brain Pituitary Kidney Adrenal Heart Vascular Tissue Adipose Tissue Angiotensinogen and the Acute‐Phase Reaction Angiotensinogen and Essential Hypertension Angiotensinogen and Preeclampsia Angiotensinogen and Heart Disease Summary

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Effects of intracerebroventricular captopril on angiotensin-converting enzyme and angiotensinogen mRNA levels in rat brain

Cited by 3 publications

References 9 publications

Octreotide-induced drinking, vasopressin, and pressure responses: role of central angiotensin and ACh

Octreotide-induced drinking, vasopressin, and pressure responses: role of central angiotensin and ACh

CHROMOSOME 17q23: A LOCUS FOR CARDIOVASCULAR DISEASE

Angiotensinogen

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