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Biomedical subjects

P Schelling

Publications and source records attributed to P Schelling.

47 records · Page 3Linked to original sources
PubMed1976

Effect of intraventricular perfusion of angiotensin II in conscious normal rats and in rats with hereditary hypothalamic diabetes insipidus.

1. Artificial cerebrospinal fluid was perfused through the cerebral ventricles of conscious rats. A basal secretion rate of 16 +/- 3 X 10(-15) mol of immunoreactive angiotensin II/min was calculated for intact rats. 2. Most of the immunoreactive angiotensin II consisted probably of the heptapeptide or pentapeptide angiotensin II fragments. 3. The pressor response to intraventricular perfusions of angiotensin II were normal in Long-Evans rats, virtually absent in rats homozygous for hereditary hypothalamic diabetes insipidus, irrespective of whether they were injected with vasopressin tannate or not, and intermediate in rats heterozygous for hypothalamic diabetes insipidus. 4. The results suggest that the pressor response to intraventricular angiotensin II is related to the release of vasopressin.

Angiotensin II↗
PubMed1976

Impermeability of the blood-cerebrospinal fluid barrier for angiotensin II in rats.

1. Anaesthetized, nephrectomized rats were infused intravenously with unlabelled angiotensin II (AII) or with [3H]angiotensin II (3H-labelled AII). The brain ventricular system was perfused with artificial cerebrospinal fluid. The perfusate was collected from the cisterna magna and analysed for AII by radioimmunological and biochemical methods. 2. No increase of immunoreactive AII in cerebrospinal fluid could be shown during intravenous infusion of AII. 3. During intravenous infusions of 3H-labelled AII at pressor doses small amounts of radioactivity were found in cerebrospinal fluid perfusate. 4. The radioactivity of cerebrospinal fluid outflow could not be related to AII.

Angiotensin II↗
PubMed1976

Pressor action of centrally perfused angiotensin II in rats with hereditary hypothalamic diabetes insipidus.

A method was devised for the perfusion of the cerebral ventricles in conscious rats. Using this method a basal secretion rate of 15 +/- 3 pg of immunoreactive angiotensin II per min was calculated. This material was suggested to be of extrarenal origin. In comparison to findings in normal Long-Evans rats, pressor responses to intraventricular perfusions of angiotensin II were reduced in rats heterozygous for hypothalamic diabetes insipidus and virtually absent in rats homozygous for the hypothalamic deficiency whether they were treated with vasopressin or not. The pressor response to intraventricular angiotensin II is suggested to be related to the release of vasopressin.

Angiotensin II↗
PubMed1976

Central pressor actions of angiotensin II.

Involvement of the area postrema in experimental hypertension has been investigated. Ablation of the rear apex of the fourth brain ventricle (=the region of the area postrema) elevated blood pressure, heart rate and plasma angiotensin II level. The same characteristic changes were seen in the two kidney Goldblatt rat model of hypertension. A possible involvement of the area postrema in this model of hypertension is discussed. Intraventricular perfusion of angiotensin II elevated blood pressure without a significant change in heart rates. This pressor response appeared to be dependent on release of antidiuretic hormone. The results are discussed in relation to the intrinsic brain angiotensinogenase system.

Angiotensin II↗
PubMed1975

The intrinsic brain iso-renin--angiotensin system in the rat: its possible role in central mechanisms of blood pressure regulation.

1. Angiotensin is produced by the intrinsic isorenin--angiotensin system. 2. Angiotensin is secreted into the cerebrospinal fluid of nephrectomized rats. 3. Angiotensin in cerebrospinal fluid elevates systemic blood pressure. 4. Rats with hereditary diabetes insipidus are virtually non-responsive to intraventricular angiotensin. 5. Angiotensin II is elevated in the cerebrospinal fluid of spontaneously hypertensive rats. 6. An intraventricular perfusion of the angiotensin II receptor-blocking agent P 113 decreases blood pressure in spontaneously hypertensive rats.

Angiotensin II↗
PubMed1975

The renin and iso-renin-angiotensin system in rats with experimental pitutary tumors (38585).

Renin, iso-renin, angiotensin I. angiotensin-converting enzyme, and angiotensinases were measured in plasma and in various extrarenal tissues of rats. Despite complete suppression of plasma renin in rats bearing pituitary tumors iso-renin and all other components of the renin-angiotensin system were found to be at or above control concentrations. The results strongly suggest that there is local synthesis of iso-renin in extrarenal tissues.

Adrenal Glands↗
PubMedDate not supplied

Involvement of ATP-sensitive potassium channels in preconditioning protection.

Single or multiple brief periods of ischemia (preconditioning, PC) have been shown to protect the myocardium from infarction during a subsequent more prolonged ischemic insult. To test the hypothesis that opening of ATP-sensitive potassium channels (KATP) is involved in this mechanism, either bimakalim, a KATP channel opener, or glibenclamide, a KATP channel blocker, were administered to mimic or to block preconditioning protection in barbital-anesthetized pigs. PC was elicited by a single period of 10 min left anterior descending coronary artery (LADCA) occlusion followed by 15 min of reperfusion before the LADCA was reoccluded for 60 min. Instead of PC, bimakalim infusion was started 15 min before the 60 min LADCA occlusion (TCO) and stopped with the onset of ischemia. Glibenclamide was administered either for 10 min prior to the PC protocol, before bimakalim infusion, or before TCO. Regional wall function was quantified with ultrasonic crystals aligned to measure wall thickening (% delta WT). At the end of the protocol, infarct size was determined by incubating myocardium with p-nitrobluetetrazolium. In seven preconditioned pigs, infarct size was 9.9 +/- 5.1% of the risk region compared with 65.9 +/- 6.0% in the seven control pigs subjected to 60 min of ischemia only (p < 0.001). In seven pigs treated with bimakalim, infarct size was reduced to 35.3 +/- 6.6 (p < 0.05 vs. controls). Blocking ATP-sensitive potassium channels with glibenclamide prior to PC abolished its protective effect (infarct size, 62.2 +/- 4.5%; p < 0.001 vs. PC alone). Glibenclamide also antagonized the protective effect of bimakalim (infarct size, 55.2 +/- 4.0%), but did not affect infarct size, when solely administered prior to the prolonged ischemic period (62.2 +/- 4.3%). We conclude that in swine myocardium KATP channels are involved in the protective effect of ischemic preconditioning, since glibenclamide completely abolished the protective effect of preconditioning, while bimakalim could--at least in part--mimic it.

Animals↗
PubMedDate not supplied

Influence of captopril treatment on angiotensin II receptors and angiotensinogen in the brain of spontaneously hypertensive rats.

The brain renin-angiotensin system (RAS) has been suggested as contributing to the pathogenesis of spontaneous hypertension in rats. Brain angiotensinogen- and angiotensin II (AII)-sensitive neurons were therefore investigated in stroke-prone spontaneously hypertensive rats (SHR-sp) and in Wistar-Kyoto (WKY) rats with and without treatment by captopril (CAP). Angiotensinogen was decreased in the anterior hypothalamus but increased in the cortex, the hippocampus, and cerebellum of SHR-sp. There were no differences between SHR-sp and WKY rats concerning the angiotensinogen content of posterior hypothalamus, brain stem, and septum. The sensitivity of the septal neurons to microiontophoretically applied AII was elevated, however, in SHR-sp as compared to WKY rats with regard to threshold and maximal response for AII-evoked neuronal discharges. The excitation characteristics did not change with the age of animals in both WKY rats and SHR-sp. The treatment of SHR-sp with CAP (50 mg/kg/day per os) starting in weanlings kept animals normotensive and reduced the high sensitivity of septal neurons to AII. Simultaneously angiotensinogen content was increased in the anterior hypothalamus and suppressed in the hippocampus. The same treatment of WKY rats reduced blood pressure somewhat and increased the angiotensinogen content in the anterior hypothalamus without affecting the neuronal sensitivity to AII. Thus, malfunction of the brain RAS may participate in the hypertension of SHR-sp, since converting enzyme blockade with CAP inhibited the blood pressure rise, augmented the angiotensinogen content of the anterior hypothalamus, and decreased the sensitivity of AII receptors in the brains of these rats.

Angiotensin II↗