Search PubMed⌕ Search

Biomedical subjects

W Rascher

Publications and source records attributed to W Rascher.

At least 271 records · Page 15Linked to original sources
PubMed1981

Thirst in the rat after ligation of the inferior vena cava: role of angiotensin II.

The role of angiotensin II in thirst states after ligation of the inferior vena cava above (CLA) or below (CLB) the origin of the renal veins as compared to sham operated controls was evaluated 24 hrs after ligation. Water intake was enhanced in CLB rats and even more so in CLA rats. Plasma angiotensin II and urea concentrations and serum osmolality were increased in CLA rats. Plasma sodium concentration and hematocrit were reduced in CLA rats, and hematocrit in CLB rats as well. Water intake in CLA rats was retarded by IV infusions of saralasin. Saralasin infusions in CLA rats resulted in a dramatic increase of plasma angiotensin II concentrations. Ligation of the inferior vena cava induces major changes in body fluid homeostasis, which are more pronounced in CLA than in CLB rats. The increase in water intake in CLA rats appears to be partly mediated by angiotensin II.

Angiotensin II↗
PubMed1981

Vasopressin in the plasma of stroke-prone spontaneously hypertensive rats.

1. Plasma concentration of arginine vasopressin, plasma osmolality and packed cell volume were measured in stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto (WKY) rats at different ages. 2. In young and in adolescent SHRSP, at 6, 9 and 12 weeks of age, plasma concentration of vasopressin was diminished as compared with age-matched WKY rats (P less than 0.01), whereas, in 18-week-old rats, the difference was not significant (P greater than 0.05). In contrast, in 24-week-old rats, plasma vasopressin was elevated as compared with WKY rats of the same age (P less than 0.01). 3. In none of the age groups did plasma osmolality differ between the two strains of rats, but in all groups packed cell volume in SHRSP was higher than in WKY rats. 4. During a 48 h period of dehydration, plasma vasopressin concentrations increased similarly in SHRSP and in WKY rats of 6 and 12 weeks of age respectively. 5. It is concluded that vasopressin does not contribute to the development of high blood pressure in SHRSP rats. The reduced plasma concentration of vasopressin may account for the decreased plasma and blood volume and the slightly elevated plasma sodium concentration observed in young SHRSP rats.

Animals↗
PubMed1981

Partial replacement of sodium by potassium in the diet restores impaired noradrenaline inactivation and lowers blood pressure in stroke-prone spontaneously hypertensive rats.

1. Partial replacement of sodium by potassium in the diet attenuates the rise in blood pressure in stroke-prone spontaneously hypertensive rats (SHR-SP). 2. The blood pressure-lowering effect of potassium cannot be ascribed to a reduction in intravascular volume. 3. The increased dietary intake of potassium leads to a reduced stimulation of the sympathoneuronal and sympathoadrenal system by cold compared with the response of sodium-loaded rats. 4. The impaired inactivation of noradrenaline observed in sodium-loaded SHR-SP is improved in SHR-SP on a potassium-substituted diet. 5. It is concluded that changes in dietary intake of sodium and potassium modulate sympathetic activity and the metabolism of noradrenaline, both of which are related to the development of hypertension in SHR-SP.

Animals↗
PubMed1981

Vasopressin-induced increase in total peripheral resistance in deoxycorticosterone acetate hypertensive rats is buffered by the baroreceptor reflex.

1. The role of arginine-vasopressin (AVP) in the maintenance of high blood pressure in rats with deoxycorticosterone acetate (DOCA) hypertension was investigated. 2. Plasma concentrations of AVP were significantly elevated in DOCa hypertensive rats compared with normotensive control rats, whether or not they received 1% sodium chloride solution or demineralized water to drink. 3. The specific antagonist of the vasopressor response to AVP, d(CH2)5VDAVP (100 microgram/kg intravenously), significantly increased cardiac output and decreased total peripheral resistance, but had no effect on mean arterial pressure in DOCA hypertensive rats. No changes of mean arterial pressure, cardiac output and total peripheral resistance were observed in the normotensive control groups after d(CH2)5VDAVP. 4. After sino-aortic baroreceptor deafferentation, d(CH2)5VDAVP decreased mean arterial pressure in DOCA--salt hypertensive rats, but not in the control groups. 5. It is concluded that elevated circulating AVP causes vasoconstriction in DOCA hypertensive rats. The AVP-induced increase in total peripheral resistance is counter-regulated by an activation of the baroreceptor reflex and subsequent reduction in cardiac output.

Animals↗
PubMed1981

Plasma angiotensin II concentrations and experimentally induced thirst.

The systemic administration of angiotensin II or its precursors will result in increased water intake. Several manipulations that result in hypovolemia and/or hypotension (extracellular thirst challenges) are known to activate the peripheral renin-angiotensin system and also produce drinking. Although there are without question multiple mediators of thirst associated with extracellular thirst challenges, one of the major factors responsible for water intake has been hypothesized to be the action of angiotensin II. In the experimental analysis of thirst, several types of hypovolemic-hypotensive manipulations have been employed. However, there is a paucity of data available that characterize the systematic changes of angiotensin II levels following such challenges. The present studies determined plasma angiotensin II levels and drinking responses after isoproterenol administration, caval ligation, and subcutaneous polyethylene glycol treatment. The experimental protocols for treatment of the animals closely approximated conditions commonly employed in the experimental analysis of thirst. The results indicated that endogenous levels of angiotensin II increase after these treatments to levels that in all likelihood are sufficient to make a substantial contribution to the drinking response.

Angiotensin II↗
PubMed1981

Effects of sodium loading, desoxycorticosterone acetate, and corticosterone on urinary kallikrein excretion.

In male Sprague-Dawley rats, changes in kallikrein activity in urine were produced by high sodium intake (1% saline as drinking fluid for 14 days), and administration of desoxycorticosterone acetate (DOCA, 15 mg/kg s.c. for 5 days), and of corticosterone (2 x 0.2 or 2 x 20 mg/kg s.c. daily for 5 days). Salt loading caused a decrease in urinary kallikrein excretion (p less than 0.005), while DOCA produced an increase (p less than 0.001). While corticosterone, administered in the low dose, had no effect on urinary kallikrein excretion, the high dose, given for 5 days, diminished kallikrein excretion to about half the basal value (p less than 0.001). Simultaneously, the excretion of aldosterone decreased to about one third the amount measured in the corresponding control rats.

Aldosterone↗
PubMed1981

The renal kallikrein-kinin system in Brattleboro rats with hereditary hypothalamic diabetes insipidus. Missing relationship between antidiuretic hormone and the renal kallikrein-kinin system.

The activity of the renal kallikrein-kinin system was investigated in male Brattleboro rats homozygous for hypothalamic diabetes insipidus (DI); Long-Evans rats (LE) were taken as controls. In the rats with DI, urinary kallikrein excretion was lower (P less than 0.05) than in the LE rats. However, when related to total renal mass or to body weight, there was no difference between the two strains. Kallikrein activity in the renal cortex was similar in the Brattleboro and the LE rats. Antidiuretic hormone (vasopressin tannate) in a dose of 100 mU given once daily for 3 days had no effect on urinary kallikrein excretion in either of the strains. Water deprivation for 24 h resulted, also in both strains, in a similar reduction in urinary kallikrein excretion. The renal kallikrein-kinin system of LE rats and that of DI rats does not principally differ in basic activity, nor in response to the administration of vasopressin, nor to water deprivation.

Angiotensin II↗
PubMed1980

Reversal of corticosterone-induced supersensitivity of vascular smooth muscle to noradrenaline by arachidonic acid and prostacyclin.

In the isolated perfused hindlimb preparation of rats treated with corticosterone (2 x 20 mg/kg daily for 2 days), the dose-response curve to noradrenaline was shifted to the left, indicating supersensitivity of the vascular bed to noradrenaline. Perfusion with arachidonic acid (10(-5) M) and prostacyclin (10(-9) M) for 5 min reversed the supersensitivity induced by corticosterone. The metabolite of prostacyclin, 6-keto PGF1 alpha(10(-9) M), was ineffective in this respect. In rats which had received desoxycorticosterone acetate (2 x 5 mg/kg daily for 7 days), there was supersensitivity of the hindlimb preparation to noradrenaline similar to that in corticosterone-treated rats. In that case, however, administration of arachidonic acid did not reverse the leftward shift of the dose-response curve. Administration of indomethacin (2 x 2.5 mg/kg for 7 days) prior to the perfusion experiment also resulted in a shift of the noradrenaline dose-response curve to the left, which was less pronounced than the shift induced by corticosterone. Combined administration of corticosterone and indomethacin caused the same increase in noradrenaline sensitivity as did corticosterone alone. Since glucocorticoids inhibit the release of arachidonic acid from phospholipids, it is concluded that corticosterone may enhance the sensitivity to noradrenaline by affecting the biosynthesis of prostaglandins.

Animals↗
PubMed1980

Increased kallikrein excretion in spontaneously hypertensive rats and its inhibition by 6-hydroxydopamine.

Urinary kallikrein excretion was studied in young, stroke-prone, spontaneously hypertensive rats (spSHR). Seven-week-old spSHR were found to excrete more kallikrein into the urine than normotensive Wistar Kyoto control rats (WKR). "Chemical sympathectomy", induced by 6-hydroxydopamine (6-OHDA) immediately after birth, resulted in normotensive blood-pressure levels and in a reduction of kallikrein in spSHR. In normotensive WKR, blood pressure and urinary kallikrein excretion were only slightly diminished by 6-OHDA. The results suggest a relationship between sympathetic activity and kallikrein excretion, being especially pronounced in spSHR, which have an elevated sympathetic activity.

Animals↗
PubMed1980

Brain angiotensin II stimulates release of pituitary hormones, plasma catecholamines and increases blood pressure in dogs.

1. The mechanisms of central angiotensin II blood pressure effects in conscious dogs on normal or sodium-deficient diets were examined. 2. The biosynthesis of brain angiotensin II in cerebrospinal fluid from its local precursor angiotensinogen was induced in vivo by injection of 0.5 unit of hog kidney renin through a chronically implanted cannula into the third brain ventricle in conscious dogs. 3. Intracerebroventricular administration of renin induced an increase of arterial blood pressure and a marked drinking response under both dietary regimens. Sodium restriction had no effect on the magnitude of the central angiotensin pressor response. 4. Plasma concentrations of renin and angiotensin II decreased, and plasma antidiuretic hormone, noradrenaline, adrenaline and corticosterone increased, in both groups of dogs. 5. Simultaneous intraventricular administrations of captopril with renin inhibited the central renin effects. Intracerebroventricular injections of [Sar1, Val5, Ala8] angiotensin II alone increased plasma renin and angiotensin II concentrations. 6. It is concluded that endogenous brain angiotensin II participates in central mechanisms of blood pressure regulation by the stimulation of the release of antidiuretic hormone, adrenocorticotrophic hormone, adrenaline and noradrenaline.

Angiotensin II↗
PubMed1980

Enhanced sympathetic activity caused by salt loading in spontaneously hypertensive rats.

1. Salt loading accelerates and increases the rise in blood pressure (spSH) in stroke-prone spontaneously hypertensive rats, but not in Wistar-Kyoto (WK) rats. 2. In both strains a slight increase in plasma volume was obtained during salt loading. 3. Salt loading caused a distinct increase in plasma noradrenaline concentration in spSH rats, but a slight decrease in WK rats. Plasma adrenaline and dopamine concentrations remained unaffected. 4. Exposure to cold resulted in a more marked stimulation of sympathoadrenal and sympathoneuronal activity in salt-loaded spSH rats than in spSH rats on a normal sodium diet. 5. It is concluded that salt loading results in a further increase of the already elevated sympathetic activity in spSH rats.

Aging↗
PubMed1980

Plasma catecholamine levels and vascular response in deoxycorticosterone acetate hypertension of rats.

1. In rats with deoxycorticosterone acetate (DOCA) hypertension basal plasma concentrations of noradrenaline and adrenaline correspond to those of sham-treated controls. 2. In DOCA-treated rats frusemide caused a more pronounced increase in plasma noradrenaline than in control rats. This difference was not observed for adrenaline. 3. In the isolated perfused hind-limb preparation the sensitivity to noradrenaline was already enhanced before blood pressure was elevated. 4. These results suggest that the adrenergic vascular tone is increased in DOCA hypertension in rats.

Animals↗
PubMed1979

Catecholamine turnover changes in hypothalamus and dorsal midline area of the caudal medulla oblongata of spontaneously hypertensive rats.

The central noradrenaline (NA) and adrenaline (A) turnover in 15--16-week-old stroke prone, spontaneously hypertensive (sp-SH) female rats in an advanced stage of hypertension was found to differ from that of normotensive Wistar-Kyoto (WKy) control rats. The catecholamine (CA) levels were measured after inhibition of dopamine-beta-hydroxylase (DBH) or phenylethanolamine-N-methyltransferase (PNMT). in the hypertensive rats the dopamine (DA) and NA levels and the NA turnover were reduced in the hypothalamus, while in the dorsal part of the caudal medulla oblongata NA levels and A turnover were reduced. Changes in hypothalamic DA and NA mechanisms and in A mechanisms in medulla oblongata may therefore be of importance in the blood pressure regulation of sp-SH rats.

Animals↗
PubMed1979

Effects of an orally active converting-enzyme inhibitor, SQ 14225, on pressor responses to angiotensin administered into the brain ventricles of spontaneously hypertensive rats.

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.

Administration, Oral↗