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Biomedical subjects

W Rascher

Publications and source records attributed to W Rascher.

At least 253 records · Page 14Linked to original sources
PubMed1982

Dissociation between in vivo and in vitro measurements of converting enzyme activity after chronic oral treatment with captopril in rats.

Intravenous administration of captopril (20 micrograms) produced inhibition of angiontensin I pressor responses by 70 percent and of plasma-converting enzyme activity by 72 percent. Oral treatment with captopril (50 mg/kg/day) for 1 week inhibited angiotensin I pressor responses more (84 percent) than plasma-converting enzyme activity (23 percent). Four month oral treatment of normotensive and spontaneously hypertensive rats with captopril (50 mg/kg/day) led to 68 and 71 percent inhibition of angiotensin I pressor responses, but produced increases in plasma-converting enzyme activity of 123 and 94 percent, respectively. In spontaneously hypertensive rats, elevated converting enzyme activity in the medulla oblongata was measured after this treatment. It is concluded that plasma-converting enzyme activity measurements can be dissociated from the in vivo inhibition of converting enzyme. Chronic oral captopril treatment results in an induction of converting enzyme biosynthesis not only in peripheral tissue but also in the brain.

Angiotensin I↗
PubMed1982

Intracerebroventricular angiotensin II increases arterial blood pressure in rhesus monkeys by stimulation of pituitary hormones and the sympathetic nervous system.

Intracerebroventricular injections of angiotensin II in anesthetized rhesus monkeys increase systemic blood pressure and heart rate. These effects are accompanied by an increase in plasma ADH, cortisol, adrenaline and noradrenaline. Angiotensin II may participate in central mechanisms of blood pressure regulation by its stimulatory effect on the sympathetic nervous system, on ADH and on ACTH release in primates.

Angiotensin II↗
PubMed1982

SA446, a new orally active converting enzyme inhibitor: antihypertensive action and comparison with captopril in stroke-prone spontaneously hypersensitive rats.

The converting enzyme inhibitors (CEI) SA446 and Captopril (CAP) were given orally at a dose of 50 mg/kg per day to adult stroke-prone spontaneously hypertensive rats (SHRSP) over a period of four weeks. Both CEI lowered arterial blood pressure (BP) to a similar extent. CAP was more inhibitory on the plasma renin-angiotensin system (RAS) than SA446. Both CEI lowered urinary aldosterone excretion but had little (SA446) or no (CAP) natriuretic effect. CAP reduced the pressor responses to intravenous (i.v.) angiotensin I (ANG I) more (52%) than SA446 (18%) and potentiated the depressor responses to i.v. bradykinin more (fortyfold) than SA446 (tenfold). In contrast, SA446 treatment reduced the pressor responses to intracerebroventricular (i.c.v.) ANG I by 21% and led to a rise in the hypothalamic renin concentration. Oral CAP treatment for four weeks did not produce these signs of a brain converting enzyme inhibition. It is concluded that SA446 is equally as antihypertensive as CAP in SHRSP. SA446 appears to penetrate more readily into the brain and to exert its action partly through inhibition of the brain RAS which is known to be stimulated in SHRSP.

3-Mercaptopropionic Acid↗
PubMed1982

Vascular effects of parathyroid hormone (PTH).

PTH causes dose dependent transient vasodilatation in various vascular beds, specifically renal, coeliac, coronary, but not osseous. It has an acute dose-dependent hypotensive effect in the intact animal which is not mediated by alpha- or beta-adrenergic, cholinergic or histaminergic mechanisms. Aortic medial smooth muscle cells respond to PTH with an increase of cAMP, cGMP and, presumably via protein kinase, with activation of phosphorylase B kinase. The acute vasodilatory effect of PTH is antagonised by indomethacin and diclofenac as well as by ouabain, suggesting that the membrane Na-K pump and prostaglandins are involved in PTH-induced vasodilatation. Parathyroidectomy and a high calcium diet attenuate the rise of arterial pressure in experimental hypertension, pointing to some permissive effect of PTH for development hypertension. This is most likely due to long term effects of PTH on vessel wall calcium content and exchange. This chronic effect of PTH may explain the high prevalence of hypertension in patients with primary hyperparathyroidism.

Animals↗
PubMed1982

Dysfunction of the adrenergic system in phosphate depleted rats.

Plasma catecholamines and vascular response to noradrenaline were studied in phosphate depleted rats. Phosphate depletion was induced in rats by dietary phosphorus deprivation for 6 weeks. Basal plasma concentrations of noradrenaline, adrenaline and dopamine were elevated in phosphate depleted rats compared to pairfed control rats. After exposure to cold (4 degrees C, 45 min) the rise in plasma catecholamines was much more pronounced in phosphate depleted rats. In the isolated perfused rat heart, the uptake of tritiated noradrenaline was unchanged. In the isolated perfused hindlimb preparation the vascular response to noradrenaline, but not to potassium chloride and arginine-vasopressin was significantly diminished in phosphate depleted rats. It is concluded that in phosphate depletion sympathetic activity is elevated and vascular response to noradrenaline diminished.

Animals↗
PubMed1982

Vasopressin in brain of spontaneously hypertensive rats.

In stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto rats (WKY), arginine vasopressin (AVP) was measured by means of a radioimmunoassay in the plasma, the pituitary gland, the hypothalamus, and the brain stem. In 6- and 14-wk-old SHRSP, the plasma concentration of AVP was lower than in age-matched WKY (P less than 0.01), whereas it was elevated at 28 wk of age (P less than 0.01). In the pituitary of 6-wk-old SHRSP, AVP was higher than in WKY (P less than 0.05), but no such difference was found in older rats. In the hypothalamus and the brain stem, AVP content was reduced in all age groups of SHRSP. Plasma osmolality was diminished in 28-wk-old SHRSP only (P less than 0.01), whereas hematocrit in all age groups was higher in SHRSP than in WKY. It is concluded that the secretion of AVP and possibly its synthesis in the hypothalamus are reduced in SHRSP. Whether the reduced AVP content in the brain stem is related to the sustained elevation of blood pressure has to be studied further.

Aging↗
PubMed1982

Opioid peptides and blood pressure regulation.

Immunohistochemical and functional studies suggest that opioid peptides are involved in blood pressure regulation. Endorphin and enkephalins contained in the brain seem to exert their effects by mediation of cardiovascular centers in the brain stem. Additional effects on blood pressure may be exhibited by circulating opioid peptides released from the pituitary and adrenal gland which may act at both central and peripheral sites. It is expected that further studies will complete our knowledge about the interaction of opioid peptides and blood pressure regulation and will result in therapeutic applications.

Animals↗
PubMed1981

[Pathophysiology of essential hypertension. Recent findings (author's transl)].

The blood pressure is regulated by the relationship of cardiac output and peripheral resistance to each other. Both parameters are influenced by the heart, by the kidneys and by the resistance vessels. For a long time the main objective of hypertension research has been directed towards these end organs of circulatory regulation. The functional condition of the heart, kidneys and arterioles is, however, decisively controlled and integrated by the brain. The newly discovered neuropeptides of recent years seem to fulfil an important function in the central mechanisms of circulation regulation. The autonomic nervous system and the hypothalamic and hypophyseal hormones have been discussed as peripheral mediators of the cardiovascular control centers in the brain.

Angiotensin II↗
PubMed1981

Plasma catecholamines, noradrenaline metabolism and vascular response in desoxycorticosterone acetate hypertension of rats.

Mineralocorticoid hypertension was induced in male Wistar rats by the injection of desoxycorticosterone acetate (DOCA) in oily solution (2 X 5 mg/kg daily for 7 days) and of desoxycorticosterone trimethylacetate in a microcrystalline suspension (15 mg/kg every third day for 4 weeks). A 1% NaCl solution or demineralized water was given as drinking fluid. Four weeks after the beginning of treatment, mean arterial blood pressure was 161 +/- 3.8 mmHg in DOCA-saline treated and 140 +/- 5.9 mmHg in DOCA-water-treated rats. Basal plasma levels of noradrenaline and adrenaline did not differ in conscious, unrestrained DOCA-treated rats and in control rats 3, 7 and 28 days after the beginning of hormone administration. Furosemide (50 mg/kg) caused within 30 min the same degree of diuresis and natriuresis in DOCA-treated and in control rats, but the plasma noradrenaline concentration in DOCA-treated rats rose to a higher level than in the controls. The isolated perfused hearts of rats which received DOCA for 7 and 28 days, respectively, had a reduced uptake of [3H]noradrenaline as compared to the controls. In isolated perfused hindlimb preparations from rats which had received DOCA for 7 days, the dose-response curve to noradrenaline but not that to KCl was shifted to the left. However, when DOCA and saline were given for 28 days, besides a higher sensitivity to noradrenaline an increased maximum response was observed with both noradrenaline and KCl. It is concluded that adrenergic tone is enhanced during the development of DOCA hypertension. Since the changes in the sympathetic nervous system in DOCA-water-treated rats, which had a less pronounced hypertension, were similar to those in DOCA-NaCl-treated rats, alterations in adrenergic vascular tone were not directly related to the level of the blood pressure.

Animals↗
PubMed1981

Plasma-converting enzyme activity does not reflect effectiveness of oral treatment with captopril.

Intravenous Captopril (20 microgram) in rats produced similar inhibition of the pressor responses to intravenous ANG I (70%) and of plasma-converting enzyme activity (CEA) measured fluorometrically (72%). One week oral treatment with Captopril (50 mg/kg per day) inhibited ANG I pressor responses more (84%) than plasma CEA (23%). Four-month oral treatment of normotensive and spontaneously hypertensive rats with Captopril (50 mg/kg per day) led to a 68% and 71% inhibition of the ANG I pressor responses, but to a 123% and 94% increase of plasma CEA, respectively. Thus, plasma CEA measurements can be dissociated from the in vivo inhibition of converting enzyme (CE). Chronic oral Captopril treatment induces CE biosynthesis.

Angiotensin I↗
PubMed1981

Reduced content of vasopressin in the brain of spontaneously hypertensive as compared to normotensive rats.

Arginine-vasopressin (AVP) content was measured by radioimmunoassay in the plasma and brain of stroke-prone spontaneously hypertensive rats (SHRsp) and normotensive Wistar Kyoto (WKY) control rats. AVP was reduced in plasma, hypothalamus, amygdala, septum and brain stem of the hypertensive animals. In view of the possible sensitizing effect of vasopressin on the baroreceptor reflex, the reduction of this peptide in the brain stem could contribute to hypertension in SHRsp.

Animals↗
PubMed1981

Central blood pressure effects of substance P and angiotensin II: role of the sympathetic nervous system and vasopressin.

The role of the sympathetic nervous system and of arginine vasopressin (AVP) in the mediation of the central cardiovascular effects of angiotensin II (ANG II) and substance P (SP) was investigated. ANG II and SP caused dose-dependent blood pressure increases when injected into the lateral brain ventricle (i.c.v.) of conscious rats; ANG II was tenfold more potent than SP. Peripheral blockade of alpha-adrenoceptors with prazosin or blockade of the vasopressor action of AVP by the AVP antagonist d(CH2)5VDAVP both partially inhibited the pressor responses to central ANG II. Combined treatment with the two blockers produced almost complete inhibition of the central ANG I responses. Substance P injected i.c.v. produced increases in noradrenaline and adrenaline but not AVP in the plasma. Peripheral alpha-receptor blockade by prazosin reversed the central pressor effects of SP to depressor responses. The AVP antagonist did not alter the cardiovascular responses to SP. It is concluded that in conscious animals, stimulation of the sympathetic nervous system and release of AVP contribute to the central pressor action of ANG II to a similar extent and independently of each other. In contrast, the central pressor responses to SP appear to be exclusively mediated by the sympathetic nervous system without participation of AVP.

Angiotensin II↗