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Biomedical subjects

H Ohde

Publications and source records attributed to H Ohde.

34 records · Page 2Linked to original sources
PubMed1989

Direct vascular effects of 19-hydroxyandrostenedione.

A C19 steroid, 19-hydroxyandrostenedione (19-OHAD), an amplifier of the mineralocorticoid effects of aldosterone, is known to cause hypertension in rats during chronic administration. In the present study we examined the direct vasoconstrictive effects of 19-OHAD and aldosterone in vitro as a possible mechanism of their hypertensinogenic effects. Contractile responses of central ear arteries from normal male rabbits to either 19-OHAD or aldosterone were examined in Krebs' bicarbonate buffer. When given alone, neither 19-OHAD nor aldosterone consistently caused contraction of the arteries, nor did 19-OHAD amplify the contractile action of aldosterone to a detectable range. Pretreatment of the ear arteries with desipramine, an inhibitor of neuronal uptake (uptake 1) of norepinephrine (NE), resulted in significant concentration-dependent contraction by each steroid. This contraction was markedly attenuated by prazosin but not by yohimbine. Both steroids significantly potentiated the contractile reaction of the ear arteries to exogenous NE in a dose-related manner without pretreatment with desipramine, suggesting that 19-OHAD may increase vascular resistance through the inhibition of extraneuronal NE uptake (uptake 2). These results suggest that 19-OHAD is not an amplifier of aldosterone at the vascular site.

Aldosterone↗
PubMed1986

Effect of kallikrein-kinin system on calcium-vitamin D3 metabolism.

Kallikrein has been reported to stimulate callus formation and cell proliferation. It is well-known that vitamin D3 play an role on the metabolism of calcium. However, the relation between vitamin D3 and kallikrein are still poorly understood. We have studied the effect of kallikrein on calcium and vitamin D3 with canine kidney. Mongrel dogs were anesthetized with sodium pentobarbital and prepared by the method of Nakanishi et al. Drugs were infused into renal artery for 60 minutes under three different serum calcium concentrations (Exp. I, Exp. II, Exp. III). Blood samples were collected at the midpoint of the 60 minutes urine collection period. Plasma vitamin D3 concentrations were measured by the metabolites of 25-hydroxyvitamin D3 and 1 alpha,25-dihydroxyvitamin D3. 25-hydroxyvitamin D3 was estimated by competitive protein binding assay and 1 alpha,25-dihydroxyvitamin D3 was determined by radioreceptor assay after separated using HPLC. Electrolytes of sodium, potassium, chloride, calcium and phosphorus in serum and urine, plasma cyclic AMP, glomerular filtration rate, renal blood flow and blood pressure were also measured respectively. Plasma 1 alpha,25-dihydroxyvitamin D3 concentration was found to be decreased by the infusion of kallikrein (0.02 KU/kg/min) in three experimental conditions, especially in Exp. II. Bradykinin (0.02 microgram/kg/min) also caused to kallikrein-like changes of vitamin D3. It is suggested that kallikrein-kinin system is related to inhibit the mechanism of vitamin D3 activation system on kidney.

Animals↗
PubMed1984

Synergic effects of kallikrein-kinin and prostaglandins on renin release on infusion of isolated hog kidney with aldosterone.

The effects of infusion of a large amount of aldosterone into the renal artery of isolated perfused hog kidney on the release of renin, prostaglandins (PG) and kinin and the excretion of urinary kallikrein were investigated. Infusion of aldosterone at a rate of 100 ng/min (100 to 800 ng/ml of perfusate) resulted in significant releases of renin, PG (PGE2 , 6-0-PGF1 alpha), and kinin and increase in urinary kallikrein. Infusion of aldosterone and an inhibitor of kallikrein, aprotinin, decreased the releases of renin, PG and kinin and infusion of aldosterone with indomethacin decreased the release of PG but increased that of kinin and urinary kallikrein without significant change in renin releases. These findings suggest that the release of renin by aldosterone may result from synergic effects of renal PG and the kallikrein -kinin system.

Aldosterone↗
PubMed1983

Effect of captopril on renal vascular resistance, renin, prostaglandins and kinin in the isolated perfused kidney.

Vasodilatory and natriuretic effects of captopril were studied in the isolated hog kidney perfused with modified Krebs-Ringer solution. Renal arterial infusion of captopril caused increases in releases of renin, prostaglandins (PGE2, 6-keto-PGF1 alpha and PGF2 alpha) and kinin, and was accompanied by a decrease in the renal vascular resistance and an increase in urinary sodium excretion. Indomethacin administered with captopril diminished the saluretic effect of captopril and evoked an increase in kinin, but was associated with a marked decrease in prostaglandin and renin releases, while renal vascular resistance remained decreased. Indomethacin alone did not alter vascular resistance and kinin; however, renin and prostaglandin releases were decreased. Aprotinin administered with captopril showed a decrease in releases of prostaglandins, renin and kinin without any change in vascular resistance. These results suggest that increased release of kinin induced by captopril contributes to a reduction in renal vascular resistance. Increased prostaglandin release after captopril administration may be caused by an increase in kinin without direct involvement of captopril in prostaglandin synthesis. Renal prostaglandins may enhance sodium excretion and mediate renin secretion in captopril perfusion.

Animals↗
PubMed1982

Effect of prostacyclin infusion on active and inactive renin release in the isolated perfused kidney.

The effect of prostacyclin infusion into the renal artery of the isolated perfused hog kidney on the release of active and inactive renin was investigated. Infusion of prostacyclin at a rate of 0.1 microgram/min resulted in a significant increase (p less than 0.01) in active renin and a significant fall (p less than 0.01) in inactive renin. Prostacyclin also increased urinary kallikrein excretion (p less than 0.05). The results indicate that the kidney secretes not only active renin but also inactive renin, and suggest that prostacyclin stimulates the conversion of inactive renin to the active form through the activation of the renal kallikrein system.

Animals↗
PubMed1982

Responses of active and inactive plasma renin and changes in urinary kallikrein and plasma prekallikrein to various conditions in normal subjects.

Little is known about changes in inactive plasma renin in various conditions or the in vivo activation mechanism of inactive renin. The effects of various factors known to stimulate or suppress renin release on active and inactive PRA were examined in normal subjects. Inactive PRA was determined as the difference between the total PRA after trypsin activation and active PRA. Concurrent measurements of urinary kallikrein excretion and plasma prekallikrein activity were performed to assess the possible role of renal or plasma kallikrein in in vivo activation of inactive renin. Short term stimulation with iv furosemide and ambulation, infusion of isoproterenol, and administration of captopril increased active PRA, but had little or no effect on inactive PRA. Sodium restriction and sodium loading, each for 4 days, induced parallel changes in active and inactive PRA. The administration of propranolol for 4 days decreased active PRA but did not change inactive PRA. There were no significant correlations between the changes in urinary kallikrein excretion and those in active PRA or in the proportion of active to total PRA after any short term treatments, except furosemide administration. Plasma prekallikrein activity was correlated with the proportion of active renin only during the long term sodium balance study. The present data suggest that the mechanisms ofr the control of inactive and active renin are different. Neither renal nor plasma kallikrein seems to be consistently involved in the in vivo activation of inactive renin.

Adult↗
PubMed1982

Evaluation of hypotensive mechanisms of captopril in addition to its inhibition of the converting enzyme in spontaneously hypertensive rats.

In spontaneoulsy hypertensive rats (SHR), the hypotensive effect of captopril (30 mg/kg/day per os for 4 days), which inhibits the converting enzyme when given orally was significantly potentiated rather than suppressed by aprotonin (100,000 KIU/day s.c. for 7 days), but was not affected by indomethacin. These findings suggest that neither the kallikrein-kinin system nor the prostaglandin system is involved in any of the hypotensive actions of captopril in SHR other than the inhibition of the converting enzyme.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

Release of prostaglandin I2 from hog kidney by propranolol.

Prostaglandin I2 (PGI2) decreases blood pressure. Perfusion of isolated hog kidney by propranolol in modified Krebs-Ringer solution resulted in a significant increase in 6-keto-prostaglandin F1 alpha, the major metabolite of PGI2. Prostaglandin E2 and renin activity remained unchanged. Because the concentration of PGI2-like substance in the renal vein has been shown to be greater than in the renal artery after bradykinin infusion, a contribution of PGI2 to the regulation of blood pressure was proposed. Isoproterenol has been shown to augment urinary kallikrein, but the effect of urinary kallikrein on propranolol is unclear. With a modified Krebs-Ringer solution free of plasma kininogen, a renin substrate, it was concluded that propranolol (1) induces PGI2 release from the kidney, which may contribute to a direct antihypertensive action of this beta-adrenergic blocking agent, and (2) decreases urinary kallikrein.

Animals↗
PubMed1981

Hormonal responses to long-term converting enzyme inhibition in hypertensive patients.

Captopril was given alone and in combination with diuretics to 49 patients with hypertension for 1 to 12 mol Within 2 mo blood pressure reduction correlated with pretreatment plasma renin activity and response to the infusion of angiotensin II antagonist, but these effects were not present at 4 mo. Plasma and urinary aldosterone were suppressed but serum converting enzyme activity, plasma bradykinin, kallikren, and prostaglandins (E and F) were in the normal range effect of captopril. Despite sustained reduction of blood pressure, plasma catecholamines were not elevated and urinary catecholamines were suppressed in patients on captopril alone. It is concluded that another mechanism, such as enhancement of renal or local kinin-prostaglandin system, as well as suppression of the renin-angiotensin-aldosterone system may be involved in the long-term efficacy of captopril. Sympathetic activity may also be depressed and contribute to the hypotensive effect.

Adolescent↗
PubMed1981

The effect of aging on urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension.

The effect of aging on urinary kallikrein excretion (UkalV) was investigated in 54 normal subjects, 11-88 yr old, and 37 patients with essential hypertension, 17-82 yr old. Urinary sodium, potassium, and aldosterone excretion (U(Ald)V) were also measured in these subjects. Urinary sodium and potassium excretion in both normal subjects and hypertensive patients did not significantly change with aging. In normal subjects, U(kal)V (r = 0.45; P less than 0.001) and U(Ald)V (r = 0.58; P less than 0.01) significantly decreased with increasing age. U(kal)V was positively correlated with U(Ald)V (r = 0.44; P less than 0.001). In contrast, the hypertensive patients had a significant decrease with age in U(Ald)V (r = -0.36; P less than 0.05), but no significant age-related change in U(kal)V. No significant correlation between U(kal)V and U(Ald)V was observed in the hypertensive patients. In individuals less than 60 yr old, there was no significant difference in U(kal)V values between normal subjects and hypertensive patients. Hypertensive patients more than 60 yr old excreted more urinary kallikrein than normal subjects of the same age group (P less than 0.05). In conclusion, the age-related decrease of U(kal)V in normal subjects may be due to the reduced activity of the renin-angiotensin-aldosterone system. It remains to be elucidated whether the absence of the age-related decrease in U(kal)V in hypertensive patients is related to the pathogenesis or pathophysiology of essential hypertension.

Adolescent↗
PubMedDate not supplied

Determination of the minimum anesthetic concentration and cardiovascular dose response for sevoflurane in chickens during controlled ventilation.

OBJECTIVE: To determine the minimum anesthetic concentration for sevoflurane and effects of various multiples of minimum anesthetic concentration on arterial pressure and heart rate during controlled ventilation in chickens. STUDY DESIGN: Prospective experimental study. ANIMALS: Seven healthy chickens, 6 to 8 months old, weighing 1.6 to 3.4 kg. METHODS: A rebreathing, semiclosed anesthetic circuit was used. Anesthesia was induced by mask with sevoflurane in oxygen. Each chicken was endotracheally intubated, then controlled ventilation was started and the end-tidal CO2 partial pressure was maintained at 30 to 40 mm Hg. Body temperature was maintained at 39.5 degrees to 41.0 degrees C. The inspired and end-tidal sevoflurane concentration were monitored with a multigas monitor. Minimum anesthetic concentration was determined as the minimal end-tidal sevoflurane concentration which prevented gross purposeful movement in response to clamping a toe for 1 minute. After the determination, the cardiovascular effects of sevoflurane at 1.0, 1.5, and 2.0 times the minimum anesthetic concentration were determined. RESULTS: The minimum anesthetic concentration for sevoflurane was 2.21% + 0.32% (mean +/- SD). Mean arterial pressure and heart rate at minimum anesthetic concentration were 84 +/- 13 mm Hg and 150 +/- 58 beats/min, respectively. There was a dose-dependent decrease in arterial pressure. The heart rate did not change significantly over the range 1 to 2 x minimum anesthetic concentration. No cardiac arrhythmias developed throughout the experiments. CONCLUSIONS AND CLINICAL RELEVANCE: The minimum anesthetic concentration for sevoflurane in chickens was within the range of minimum alveolar concentration reported in mammals. When the concentration of sevoflurane is increased during controlled ventilation in chickens, decrease in arterial pressure should be expected.

Anesthetics, Inhalation↗