Interferences with the Renin-Angiotensin System and Their Effects on High Blood Pressure

Ganten, Detlev; Gross, F.

doi:10.1007/978-3-642-66309-3_11

Cited by 4 publications

(2 citation statements)

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“…The development of various inhibitors has resulted in a more rational approach to the pathophysiology, diagnosis and perhaps treatment of conditions that are characterized by increased activity of the RAS (for review see [11,83]). the kininogenase-kinin system).…”

Section: Interferences With the Ras And Angiotensin Receptorsmentioning

confidence: 99%

The renin-angiotensin-aldosterone system

Vecsei

Hackenthal²,

Ganten³

1978

Klin Wochenschr

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127

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"The present results indicate that there is a close relationship between the incretory function of the kidney, which is shown by the discharge of renin and similar materials, and the function of the adrenal cortex, especially the zona glomerulosa, which is the place of production of the sodium-retaining hormone aldosterone . Salt load inhibits the production of renin and aldosterone, while salt deprivation stimulates the production of both. The excess of sodium-retaining corticoids (DOC or aldosterone) together with sodium suppress the secretion of renin, while a deficiency of cortical hormones (adrenalectomy, morbus Addison) increase it." ... "Under these conditions the development of experimental renal hypertension could be explained as follows: the narrowing of the renal artery stimulates the secretion of renin which itself increases the formation or discharge of mineralocorticoid hormones (aldosterone or similarly acting corticoids). The resulting retention of sodium does not lead to the normal reduction of renin secretion in the ischemic kidney, so that corticoid production in the adrenal cortex is further stimulated despite no need for it."

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Section: Interferences With the Ras And Angiotensin Receptorsmentioning

confidence: 99%

The renin-angiotensin-aldosterone system

Vecsei

Hackenthal²,

Ganten³

1978

Klin Wochenschr

Self Cite

127

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“…The formation of angiotensin I (ANG I) from angiotensinogen by renin can be inhibited by pepstatin and by competitive substrate analogues. The conversion of ANG I into ANG I1 is prevented by peptides such as the nonapeptide SQ 20881 (for review see Ganten & Gross, 1977). Recently, a new converting-enzyme inhibitor, SQ 14225, has been synthesized.…”

Section: Introductionmentioning

confidence: 99%

Effects of an Orally Active Converting-Enzyme Inhibitor, SQ 14225, on Pressor Responses to Angiotensin Administered into the Brain Ventricles of Spontaneously Hypertensive Rats

et al. 1979

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1. Two hours after oral feeding of normotensive Wistar Kyoto rats with the converting-enzyme inhibitor SQ 14225 (1 and 10 mg/kg), an increase of angiotensin I plasma concentrations from 892 +/- 113 to 1660 +/- 167 and 2951 +/- 405 pg/ml was observed. 2. Administration of SQ 14225 with the drinking fluid overnight suppressed the pressor responses to intravenous angiotensin I, although the blood pressure increase after intravenous angiotensin II was not altered in normotensive and spontaneously hypertensive rats. No change of pressor effects after injections of angiotensin I and II into the brain ventricles was observed after oral SQ 14225. 3. Intracerebroventricular infusions of SQ 14225 in spontaneously hypertensive rats abolished the central pressor responses to angiotensin I. 4. The results show that SQ 14225 effectively blocked the conversion of endogenous and exogenous angiotensin I into angiotensin II in plasma, and the conversion of exogenous angiotensin I in brain. Under the conditions studied, SQ 14225 does not cross the blood-cerebrospinal fluid barrier in spontaneously hypertensive rats.

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