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Biomedical subjects

J S Fan

Publications and source records attributed to J S Fan.

35 records · Page 2Linked to original sources
PubMed1981

Effect of adrenocortical steroids and their structural analogues on blood pressure in sheep.

1. A model of adrenocortical steroid-induced hypertension based on the effects of ACTH administration has been developed in sheep. The present studies examine the effects of a number of different steroid hormones on blood pressure to investigate their structure-activity relationships. 2. Infusion of the major ovine adrenal steroid hormones (combined steroid infusion of cortisol, corticosterone, 11-deoxycortisol, aldosterone, deoxycorticosterone) reproduced the metabolic but not the blood pressure effects of ACTH. 3. Addition of 17 alpha, 20 alpha-dihydroxyprogesterone and 17 alpha-hydroxyprogesterone, at rates appropriate for conditions of ACTH stimulation, to the combined steroid infusion reproduced both the blood pressure and metabolic effects of ACTH. 4. 17 alpha-20 beta-Dihydroxyprogesterone, 20 beta-dihydroxy-11-deoxycortisol and 20 beta-hydroxycortisol all had additional hypertensive activity when given with combined steroid infusion, but 16 alpha-hydroxyprogesterone, 11 beta, 17 alpha-dihydroxyprogesterone, 20 alpha-hydroxyprogesterone and 20 beta-hydroxyprogesterone did not. 5. These studies support the concept of a new class of steroid hormone action in blood pressure regulation.

Adrenal Cortex Hormones↗
PubMed1980

ACTH-elicited sodium appetite in sheep.

Intramuscular injections of long-acting synthetic ACTH (45 U twice daily for 5 days) caused a large increase in the intake of 0.5 M NaCl in sheep. Mean Na intake of the sheep on the last 3 days of treatment approximated 50% of their total extracellular fluid Na. The mineral appetite was specific for NaCl. Intakes of 0.5 M KCl or 0.25 M CaCl2 were not significantly altered. The enhanced appetite for Na induced by ACTH appeared to precede any increase in urinary Na excretion. ACTH treatment was ineffective in adrenalectomized sheep. However, an infusion into adrenalectomized sheep of a combination of adrenal steroid hormones (including aldosterone, deoxycorticosterone, 11-deoxycortisol, cortisol, and corticosterone) that contrived blood levels similar to those, obtained with ACTH treatment in normal sheep did induce Na appetite. Thus, ACTH induces a specific, adrenal-steroid hormone-dependent Na appetite in sheep.

Adrenocorticotropic Hormone↗
PubMed1978

Exaggerated natriuresis in ACTH hypertension in sheep.

Adrenocorticotrophic hormone (ACTH) administration to sheep (100 IU/day) produces a sustained increase in arterial pressure within 24 h. The effect of ACTH on excretion of an intravenous saline load was tested in 8 adult cross-bred Merino ewes. A significant diuretic response to saline loading was found after 24 h but no increased natriuresis. On days 3 and 6, diuretic and natriuretic responses were both significantly increased. Steroid-induced sodium retention may have abolished the natriuretic effect on day 1.

Adrenocorticotropic Hormone↗
PubMed1977

Measurement of extracellular fluid volume and blood volume in sheep.

Methods are described for the simultaneous measurement of extracellular fluid volume (ECFV) and plasma volume (PV) in sheep using dilution of 82Br (as sodium bromide) and 131I-labelled ovine gamma globulin. Following injection of 82Br (100 micronCi), equilibrium in blood was reached after 3 h at which time only 4% of the injected dose was in rumen water. The ECFV was measured as the mean of the 2- and 3-h bromide space after correction for the relative water content of plasma, the Gibbs-Donnan factor and the loss of 82Br into red blood cells. 131I-labelled ovine gamma globulin (20 micronCi) was injected after the 3-h 82 Br space was obtained and blood samples were taken at 10, 20, 30 and 40 min. In 16 determinations in 11 sheep (25-47 kg body weight) the mean (+/- s.e.m.) ECFV was 9112 +/- 289 ml (or 245 +/- 9 ml/kg). The mean PV for 16 observations in 11 sheep measured together with ECFV was 1597 +/- 62 ml (or 42-8 +/- 1-8 ml/kg). Although there was no relationship between body weight and PV there was a significant correlation between ECFV and body weight and also significant negative correlations between body weight and ECFV or PV when these were expressed as a function of body weight. The variation in ECFV measured on four occasions over 7-10 days in four sheep was 3-5% (range 2-6-4-6%). For PV measured in two animals on two consecutive days at the same time as ECFV the coefficient of variation was 1-5 and 2-1%. Acute sodium depletion (250-670 mmol) by parotid duct cannulation in three sheep resulted in a fall in ECFV which would account for only 15-20% of the sodium deficit. The remainder is presumably derived from ruminal sodium stores.

Animals↗
PubMed1976

Further unravelling of the causes of ACTH-induced hypertension in the sheep.

1. Acute severe sodium subtraction (20-25% of total exchangeable sodium) before or during treatment with adrenocorticotrophic hormone (ACTH) does little to modify the increase in blood pressure induced by ACTH. 2. Chronic low salt diet, less than 5 mmol/day, abolishes the blood pressure increase, but the response can be restored by increasing the sodium intake to as little as 10 mmol/day. 3. 17alpha,20alpha-Dihydroxyprogesterone infused concurrently with other adrenal steroids will mimic ACTH hypertension and perhaps represents a new class of steroid capable of influencing blood pressure.

Adrenocorticotropic Hormone↗
PubMed1975

Effect of intravenous infusion of corticosteroids on blood pressure, electrolytes, and water metabolism in sheep.

ACTH administration (80 IU/day for 5 days), which produces hypertension and charateristic metabolic effects in sheep (38), has been compared with the effect of intravenous infusion of cortisol (5 mg/h), corticosterone (0.5 mg/h), deoxycorticosterone (50 mug/h), and 11-deoxycortisol (1 mg/h), each given singly for 5 days. Further, a mixture consisting of aldosterone (3 mug/h), cortisol (5 mg/h), deoxycorticosterone (25 mug/h), corticosterone (0.5 mg/h), and 11-deoxycortisol (1 mg/h), was also infused intravenously for 5 days. In another series of experiments, 18-hydroxydeoxycorticosterone (100 mg/h) was also included in the combined-steroid solution. With the exception of 18-hydroxydeoxycorticosterone, which was not measured, the rates of infusionproduced peripheral arterial blood levels of the steroids similiar to those seen with ACTH stimulation. Blood pressure,water intake, urine output, and plasma and urinary electrolytes were measured: individual steroids had little effect on these, but manyof the metabolic changes produced by ATCH (hypokalemia and increased water intake andurine output) were produced by the combined-steroid infusion. However, the combined-steroid infusion failed to induce an increase in blood pressure similiar to that seen inthe ACTH experiments. Thus the findings are against a major role in ACTH hypertension for any steroid used, either singly or in combination. As yet unrecgnized factor/s may be involved in the ACTH-induced hypertension.

18-Hydroxydesoxycorticosterone↗
PubMedDate not supplied

The effect of corticotrophin (ACTH) administration on the pressor action of angiotensin II, noradrenaline and tyramine in sheep.

1. Pressor responses to angiotensin II, noradrenaline and tyramine were examined in sheep prior to and during the development of corticotrophin-induced hypertension. 2. Pressor responses to angiotensin II amide did not change with corticotrophin (ACTH) administration. Small significant increases in pressor responses to noradrenaline occurred at low doses only (0.27 and 1.06 mumol/h). Significant increases in response to tyramine occurred after 24h of ACTH administration, but were not maintained after 6 days of ACTH. These changes are quantitatively small and do not suggest that changes in pressor sensitivity contribute significantly to the rise in blood pressure following ACTH administration. 3. Sodium depletion significantly reduced the pressor responses to angiotensin II amide at all doses and to tyramine in the middle range only, but did not affect the responses to noradrenaline.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Blood pressure and metabolic effects of ACTH in anephric sheep.

1. ACTH (80--100 iu/day) was administered to seven sheep for 3--5 days following bilateral nephrectomy. 2. ACTH treatment produced rises in mean arterial pressure in anephric sheep similar to those observed in intact animals. Following withdrawal of ACTH, blood pressure declined over the following 72 h. 3. ACTH produced a transient fall in plasma potassium and anephric sheep, suggesting an internal redistribution mechanism for this ion. 4. These studies demonstrate that adrenal steroid hormones can modify blood pressure in the absence of the kidney.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Effect of potassium, angiotensin II and ACTH on blood aldosterone and cortisol in sheep on different dietary potassium and sodium intakes.

The short term aldosterone response to manipulations of potassium (K), angiotensin II (AII) and ACTH were examined in sheep on a variety of chronic electrolyte regimes. Reduction in Na intake increased blood aldosterone to a greater extent on 100 mmol/day K than a K-free diet. Aldosterone increased in response to AII under conditions of chronic dietary Na restriction, in contrast to acute Na depletion. The effects of K, AII, and ACTH on aldosterone concentrations in sheep on varying intakes of Na and K are similar to that reported for other species.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Role of inward and delayed rectifier currents in generation of early afterdepolarization in guinea pig ventricular myocytes under K(+)-free or low K+ superfusion.

Early afterdepolarization (EAD) was studied in isolated ventricular myocytes of guinea pig heart. Under K(+)-free's treatment, most of the myocytes showed hyperpolarization in resting potential and the duration of action potential was prolonged, eventually leading to the appearance of EAD with the second plateau of -76 +/- 3 mV. TTX (10 microM) and verapamil (10 microM) or normal Tyrode's solution abolished the EAD. The background I-V curve showed inward rectifying with a crossover in the level of -80 to -30 mV and the reversal potential shifted from -80 to -120 mV when normal Tyrode's solution was changed to K(+)-free solution. The changes of I-V relationship of inward current IK) were similar to the background ones except without crossover. The delayed rectifier current (IK) was inhibited significantly under K(+)-free treatment. Low K+ (2.7 mM) superfusion was able to induce EAD in only a few cases (4/15). Adding Cs+ (5.0 mM) into low K+ solution, EAD was induced in almost every case. The background I-V curve was inhibited slightly under low K+ superfusion, but was inhibited significantly with a remarkable crossover under low K+ and Cs+ treatment. The changes of I-V curve IK1 under low K+ or low K+ and Cs+ treatment were similar to the changes of background ones. There were no significant changes in the IK under low K+ superfusion while a remarkable inhibition occurred under low K+ and Cs+ treatment. It was suggested that both IK1 and IK were involved in the induction of EAD under K(+)-free or Cs+ treatment in guinea pig ventricular myocytes.

Action Potentials↗