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Biomedical subjects

M Handa

Publications and source records attributed to M Handa.

At least 235 records · Page 13Linked to original sources
PubMed1983

Urinary prostaglandin E2 and kallikrein excretion in glucocorticoid hypertension in rats.

1. Oral administration of dexamethasone (about 2.5 X 10(-7) mol/day) caused hypertension in rats. The blood pressure rose from 108 +/- 6 (mean +/- SD) to 156 +/- 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. In this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein-kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.

Aldosterone↗
PubMed1983

Effects of diuretics on the vasoconstrictor responses to norepinephrine and potassium ions in the rat mesenteric artery.

The effects of four different diuretics, hydroflumethiazide, furosemide, piretanide and potassium canrenoate on the vascular responses to norepinephrine and potassium chloride in the perfused rat mesenteric vascular bed have been studied. Furosemide or piretanide in the perfusate inhibited the vascular response to norepinephrine in a dose-related manner, while the vascular contraction induced by potassium chloride was not affected by these substances. In contrast to furosemide and piretanide, potassium canrenoate inhibited vascular responses to both norepinephrine and potassium ions. Hydroflumethiazide did not induce any change in the vascular response to norepinephrine or to potassium chloride. From these results, it is suggested that furosemide, piretanide and potassium canrenoate, but not hydroflumethiazide have direct vascular actions independent from their renal actions which may contribute to their antihypertensive effects.

Animals↗
PubMed1982

Mechanism of pressor effects of intraventricular injection of angiotensin II in the rat: role of vasopressin and renal nerves.

1. The role of the kidney and vasopressin in the increase of blood pressure obtained when angiotensin II is injected intraventricularly into rats has been investigated. 2. Intraventricular injection of angiotensin II led to a significant increase in blood pressure in the control and all sham-operated rats compared with that in unilaterally nephrectomized, one-kidney denervated rats and bilaterally nephrectomized rats. The degree of increase in blood pressure in unilaterally nephrectomized, one-kidney denervated rats was equal to that in bilaterally nephrectomized rats. 3. The increase in blood pressure in the bilaterally nephrectomized rats lasted significantly longer than that in the control and unilaterally nephrectomized, one-kidney denervated rats. 4. In the bilaterally nephrectomized rats plasma vasopressin was still higher 30 min after the intraventricular injection of angiotensin II than that of the control and unilaterally nephrectomized, one-kidney denervated rats. 5. These results suggest that the rise in blood pressure observed after intraventricular injection of angiotensin II is due partly to stimulation of the renal sympathetic nervous system and partly to increase in plasma vasopressin concentration.

Angiotensin II↗
PubMed1982

Role of renin-angiotensin system in glucocorticoid hypertension in rats.

The role of the renin-angiotensin system in the regulation of the blood pressure of dexamethasone-treated rats (Dex) was evaluated using saralasin, an angiotensin II antagonist, and SQ 14225 (SQ) (d-3-mercapto-2-methylpropranoyl-1-proline), an angiotensin-converting enzyme inhibitor. During a 7-day period blood pressure rose 65 +/- 10 mmHg (P less than 0.001) in Dex with no significant changes in plasma renin activity. Concurrent administration of dexamethasone and SQ attenuated the elevation of blood pressure (P less than 0.05). In the conscious, freely moving state, intravenous injection of SQ (10, 30, 100 micrograms/kg) reduced blood pressure of DEX in a dose-dependent manner (P less than 0.05). Also, intravenous injection of saralasin (10 micrograms.kg-1 . min-1) reduced blood pressure significantly (P less than 0.01). Bilateral nephrectomy abolished the effects of saralasin and SQ on blood pressure in Dex. These results indicate that the elevation of blood pressure in DEX depends partially on the renin-angiotensin system.

Animals↗
PubMed1982

Effects of magnesium on the vasoconstrictor responses to norepinephrine and potassium chloride in the rat mesenteric artery.

In the perfused rat mesenteric vascular bed, the effects of magnesium and calcium on the vasoconstrictor responses to norepinephrine or potassium chloride were studied. Higher concentrations of magnesium in the perfusate attenuated the vascular responses to norepinephrine and potassium chloride in a dose-related manner. Higher concentrations of calcium in the perfusate enhanced greatly the vascular responses to potassium chloride, while the response to norepinephrine was only slightly potentiated by increasing calcium concentration. The attenuating effect of magnesium on the responses to norepinephrine and to potassium chloride were reversed by elevation of calcium concentration in the perfusate. The potentiating effects of calcium on the responses to potassium chloride were also reversed by increasing the concentration of magnesium. However, an inhibitory effect of magnesium on the responses to norepinephrine was not observed in the presence of higher concentrations of calcium. These results indicate that magnesium acts antagonistically on calcium movement in vascular contractions due to potassium chloride, but that the relationship between magnesium and calcium is more complex in vascular contractions induced by norepinephrine.

Animals↗