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Biomedical subjects

A Knorr

Publications and source records attributed to A Knorr.

At least 91 records · Page 5Linked to original sources
PubMed1984

Differential influence of the calcium antagonist nitrendipine and the vasodilator hydralazine on normal and elevated blood pressure.

The relationship between pre-treatment blood pressure and its reduction by the calcium antagonist nitrendipine (NIT) and the vasodilator hydralazine (HYD) was studied in conscious normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR). In SHR the correlation was linear and similar after NIT and HYD. In WKY, however, the hypotensive effect of HYD was greater than that of NIT. As revealed by the dose-response curves in SHR both drugs produce similar maximal drops in blood pressure by about 54%. In WKY, HYD also caused a similar relative reduction in blood pressure. In contrast, after NIT initial blood pressure was reduced by only 27% at maximum. The greater hypotensive effect of HYD in WKY is not caused by impaired sympathetic counterregulation since in both substrains tachycardia was more prominent after HYD. Possible mechanisms of the enhanced depressor action of NIT in hypertension are discussed.

Animals↗
PubMed1983

Nitrendipine and other calcium entry blockers (calcium antagonists) in hypertension.

Nitrendipine is a calcium antagonistic 1,4-dihydropyridine derivative with a pronounced antihypertensive activity in animal experiment. Similar to other calcium entry blockers, nitrendipine decreases blood pressure by lowering the elevated peripheral vascular resistance. However, its long-term effect differs from that of vasodilators such as hydralazine and minoxidil. In contrast to vasodilators, nitrendipine reduces heart hypertrophy in various forms of experimental hypertension in rats. Nitrendipine is highly effective in normalizing blood pressure, reducing heart hypertrophy, and preventing mortality in salt-related hypertension (two-kidney renal hypertension, salt-induced hypertension in Dahl rats), which are rather refractory to the effect of vasodilators. Nitrendipine reduces renovascular resistance in spontaneously hypertensive rats but has no effect on that of normotensive rats. In conscious renal hypertensive dogs, nitrendipine decreases blood pressure more than does hydralazine. The reflex tachycardia is more pronounced after hydralazine than after nitrendipine; blood pressure decrease is greater and the duration of the effect is longer than that of nifedipine. Nitrendipine is thus predicted as an effective drug for antihypertensive monotherapy.

Animals↗
PubMed1982

Erythrocytic sodium ion transport systems in primary and secondary hypertension of the rat.

Sodium and potassium ion transport systems were studied in erythrocytes from spontaneously hypertensive Okamoto rats (SHR), hypertension-prone Sabra rats (SbH), and one-kidney one-clip Goldblatt hypertensive rats, and compared with Wistar-Kyoto normotensive rats (WKY), hypertension-resistant Sabra rats (SbN), and sham-operated Wistar rats. We observed the following: (1) An increased net potassium influx and a reduced net sodium extrusion occurred in SHR. The increased potassium influx was inhibited by ouabain, indicating an increased sodium ion pump activity. Bumetanide-sensitive sodium extrusion was lower in SHR than it was in WKY, indicating abnormally low outward sodium-potassium cotransport fluxes. (2) Passive sodium ion permeability was increased in SbH compared with SbN. Cotransport was normal in SbH rats. (3) Sodium-potassium cotransport and passive permeability were normal in renovascular hypertension. (4) After a chronic or acute sodium load, the sodium content increased in erythrocytes from SHR and SbH but not in those of normotensive or renal hypertensive rats. It appears therefore that erythrocyte membrane abnormalities leading to an increased intracellular sodium concentration are only present in genetic hypertension. The reduction of outward sodium-potassium cotransport observed in SHR is identical to that previously reported in human essential hypertension, suggesting that it may be considered as a genetic marker.

Animals↗
PubMed1982

Nisoldipine (BAY K 5552), a new calcium antagonist. Antihypertensive effect in conscious, unrestrained renal hypertensive dogs.

The antihypertensive effect of nisoldipine (BAY K 5552), a new calcium antagonist with peripheral vasodilator properties, was studied by a radio-telemetric method in conscious, unrestrained renal hypertensive dogs. Nisoldipine has a long lasting antihypertensive action (12 hr at 0.3 mg/kg p.o.) in comparison with nifedipine (6 hr at 3.15 mg/kg p.o.). Its antihypertensive efficacy is equal to that of minoxidil and superior to nifedipine, hydralazine, diltiazem and verapamil. After nisoldipine, only a short lasting initial reflex tachycardia was noted, whereas after the other vasodilators tachycardia persisted for the entire period of blood pressure reduction. Diltiazem and verapamil produced almost no tachycardia. In some cases a bradycardia was observed after high doses of verapamil.

Animals↗
PubMed1981

Furosemide and bumetanide-sensitive Na+ fluxes in erythrocytes from genetically hypertensive rats (SHR).

Na+ and K+ fluxes from erythrocytes of SHR and WKY control rats have been studied. Fluxes were measured in both fresh and sodium-loaded (after exposure to ouabain or PCMBS) erythrocytes. Pump activity appears higher and furosemide or bumetanide sensitive Na+ efflux lower in SHR compared to WKY suggesting a similar abnormality in SHR genetic hypertension as in human hypertension.

4-Chloromercuribenzenesulfonate↗
PubMed1981

Effect of a new calcium antagonist, nitrendipine, on blood pressure and heart rate of conscious, unrestrained dogs.

The acute effects of a single dose of a new calcium-antagonistic vasodilator, 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridine carboxylic acid, 3-ethyl-5-methyl ester (nitrendipine, Bay e 50090, on blood pressure and heart rate was examined in conscious dogs by means of a radio-telemetric method. Nitrendipine caused a dose-dependent fall in mean arterial blood pressure of up to 30% in renal hypertensive dogs in a dose range of 0.3-3.15 mg/kg p.o., which was maximal within 2-3 h and was maintained for up to 8 h after a single dose. In normotensive dogs, nitrendipine was somewhat less active. The fall in blood pressure was accompanied by an increase in heart rate, which was less pronounced and less persistent than after administration of hydralazine. Nitrendipine was found about 20 times more potent in its antihypertensive action than hydralazine.

Animals↗
PubMed1981

Total Na(+)- and K(+)-fluxes in erythrocytes of spontaneously and one-kidney Goldblatt hypertensive rats.

Na(+) and K(+) net fluxes were determined from Na(+)-loaded and K(+)-depleted erythrocytes of 10 weeks old female spontaneously hypertensive rats of the Okamoto/Oaki strain (SHR) and female one-kidney Goldblatt hypertensive Wistar rats. Net Na(+) extrusion was reduced to 5.60 + 0.40 mmol/l cells x hr (n=7) in SHR as compared with normotensive Wistar/Kyoto (WKY) controls (7.13+ 0.25 mmol/l cells x hr, n=6; P less than 0.05). The na(+)/K(+) net flux ratio was also lower in SHR (2.39 +0.17) than in WKY (3.39 +0.45; P less than 0.05). On the other hand, no difference could be demonstrated between net Na(+) extrusion in sham-operated Wistar rats (7.43 +0.80 mmol/l cells x hr, n=7; P less than 0.05) and four weeks after operation (9.28 +0.77 mmol/l cells x hr, n=11; P greater than 0.05). In contrast ne Na(+) extrusion even showed a tendency to rise in renal hypertensive rats. Na(+)/K(+) net flux ratios were unchanged in the three groups (3.81 +0.42, 3.28 +0.29, 3.98 +0.45; P greater than 0.05), although blood pressure was markedly increased. It is concluded that decreased net Na(+) extrusion and reduced Na(+)/K(+) net flux ratio in female Okamoto SHR are not caused by increase in blood pressure, but may be a determinant of genetic hypertension in this strain.

Animals↗
PubMed1980

Stimulation by adrenaline and dopamine but not by noradrenaline of myocardial alpha-adrenoceptors mediating positive inotropic effects in human atrial preparations.

In isolated electrically driven right auricular strips of human hearts (1 Hz at 37 degrees C) the ability of the endogenous catecholamines noradrenaline, adrenaline, and dopamine to mediate positive inotropic effects by stimulation of myocardial alpha-adrenoceptors was investigated. 1. The concentration-response curve for the positive inotropic effect of noradrenaline was shifted to the right by pindolol, 10(-8)M, whereas the additional blockade by phentolamine, 3 x 10(-6)M, was without further effect; therefore, the positive inotropic effect of noradrenaline is mediated by beta-adrenoceptors only. 2. In contrast, the positive inotropic effects of adrenaline as well as of dopamine are caused by stimulation of both, beta- and alpha-adrenoceptors. 3. These results are discussed with respect to the possible physiological and pathophysiological function of myocardial alpha-adrenoceptors.

Catecholamines↗