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Biomedical subjects

G Tolis

Publications and source records attributed to G Tolis.

At least 109 records · Page 6Linked to original sources
PubMed1977

Response of several adrenal steroids to ACTH stimulation in essential hypertension.

Plasma concentrations of progesterone (P), deoxycorticosterone (DOC), 17-hydroxyprogesterone (17-OH P), corticosterone (B), deoxycortisol (S), cortisol (F), and aldosterone were measured in 8 control subjects and in 10 patients with low and normal renin essential hypertension (EH) before and 4 and 8 h after an iv infusion of 25 units of ACTH. Secretion rates of 18-hydroxy-11-deoxycorticosterone (18-OH DOC) were measured for the 24 h prior to and the day of the ACTH infusions. The hypertensive patients had significantly higher plasma levels of aldosterone, DOC and S after ACTH than the controls, whereas plasma B levels were significantly lower. The low renin subgroup considered separately had significantly higher plasma levels of aldosterone and DOC than controls, and higher levels of B and lower levels of F than the normal renin subgroup in response to ACTH. Although not significantly different, the plasma levels of P and the secretion rate of 18-OH DOC tended to be higher, and plasma 17-OH P and F levels lower after ACTH in patients with EH than in controls. The low renin subgroup tended to have the highest plasma S levels and 18-OH DOC secretory rates and lowest F levels. Estimations of adrenal 11beta-hydroxylating efficiency in response to ACTH in patients and controls by plasma steroid ratios revealed significantly lower B/DOC ratios in both low and normal renin patients compared to controls, supported by somewhat lower F/S ratios in these patients, especially those in the low renin subgroup. Altered 17-hydroxylating efficiency seen by significantly lower 17-OH P/P ratios were also found in those with EH, supported by somewhat lower F/B and S/DOC ratios in these patients, agian especially in the low renin subgroup. These data are compatible with a pattern of altered adrenocortical steroid biosynthesis in essential hypertension bearing features similar to adrenal 11beta and 17alpha-hydroxylation deficiencies.

Adrenal Cortex Hormones↗
PubMed1977

Ineffectiveness of pyridoxine (B6) to alter secretion of growth hormone and prolactin and absence of therapeutic effects on galactorrhea-amenorrhea syndromes.

The acute effect of pyridoxine (B6) on serum GH and PRL levels and its chronic effects on galactorrhea in nine subjects (group I, n=4, idiopathic galactorrhea with normal PRL levels and normal menses; Group II, n=5, galactorrhea-amenorrhea with increased PRL levels) have been studied. Pyridoxine did not acutely alter GH or PRL levels. There was no decrease in galactorrhea, no resumption of menses and no decrease in PRL following tow months of B6 therapy. In contrast, bromocriptine was effective in suppressing galactorrhea and restoring normal menses in group II subjects and remains the therapy of choice for this purpose.

Amenorrhea↗
PubMed1976

Induction of menstruation with bromocryptine in patients with euprolactinemic amenorrhea.

Three nulliparous women presented with secondary amenorrhea with no evidence of endocrinopathy and normal skull x-ray. Pulsatile gonadotropin secretion was reduced, but an adequate pituitary gonadotropin reserve was demonstrable with luteinizing hormone-release factor provocation. The administration of bromocryptine was associated with amplification of pulsatile secretion of gonadotropins and was followed, in two of the three, by ovulatory menstruation. It is suggested that bromocryptine should be considered for induction of menstruation in euprolactinemic secondary amenorrhea.

Adult↗
PubMed1976

Elevation of serum creatine kinase in severe hypokalemic hyperaldosteronism.

The association between hypokalemia and increased serum creatine kinase has been investigated. Two patients were found who had severe hypokalemic hyperaldosteronism who had elevation of serum creatine kinase activity. The CPK activity returned to normal values after fluid and potassium replacement. In a prospective study of 129 patients with hypokalemia which did not include any patients with hyperaldosteronism, 12 were found to have increased CPK activity but each of these had some other severe disease process which could account for the increased CPK. Three other patients with K+ (2.2 MEq/1 did not have increased CPK. It is concluded that patients with severe hypokalemia such as that occurring in hyperaldosteronism with muscle weakness may have elevated CPK directly related to their hypokalemia. In other patients with hypokalemia, 10% may have increased CPK but this is related to other disease processes.

Adult↗
PubMed1976

Mineralocorticoid secretion in essential hypertension with normal and low plasma renin activity.

In 19 control subjects, 33 patients with essential hypertension and normal plasma renin activity (PRA) and 11 patients with low PRA, secretory rates of 18-hydroxy-11-deoxy-corticosterone (18-OH DOC), 11-deoxycorticosterone (DOC) and corticosterone were measured. Patients with low PRA were significantly older and had higher arterial pressure and slightly lower plasma potassium levels than patients with normal PRA. Mean 18-OH DOC secretion rate was higher in patients with normal PRA (603 +/- 112 SEM mug/24 hr) than in control subjects (219 +/- 19) and considerably higher (P less than 0.001) in patients with low PRA (1800 +/- 472). DOC and corticosterone secretion rates were within normal limits in most hypertensive patients. Plasma aldosterone was significantly higher in the hypertensive population than in control subjects whereas no significant difference was observed between the low- and normal-renin groups. A significant (P less than 0.01) mutual positive correlation was found between the secretion rates of 18-OH DOC, DOC and corticosterone in patients with low plasma renin activity. In contrast, there was no correlation between the secretion rates of the three mineralocorticoids in control subjects and patients with normal plasma renin activity. These data suggest a biosynthetic variation of the mineralocorticoid pathways in essential hypertension.

18-Hydroxycorticosterone↗
PubMed1976

Plasma cyclic adenosine 3':5'-monophosphate response to isoproterenol and glucagon in hyperkinetic borderline (labile) hypertension.

The hemodynamic changes observed in patients with the "hyperkinetic" form of borderline (labile) essential hypertension (BEH) could be related to the hyperresponsiveness of cardiac beta-adrenergic receptors to catecholamines. The isoproterenol-induced increase in plasma cyclic adenosine 3':5'-monophosphate (cAMP) reflects the response of adenylate cyclase to beta-adrenergic stimulation, whereas a non-beta-receptor-mediated increase occurs with the administration of glucagon. Both substances were infused into 13 control subjects and 14 patients with the hyperkinetic form of BEH before and after propranolol administration. Baseline plasma cAMP concentrations were comparable in both groups. After 30 minutes of isoproterenol infusion (20 ng/kg per min) a significantly higher increase in plasma cAMP and heart rate and a smaller decrease in diastolic blood pressure were seen in this type of BEH than in control subjects. The increase in plasma cAMP and in heart rate correlated positively when all subjects were considered together. Propranolol abolished hemodynamic and humoral responses to a similar degree in both groups. The plasma cAMP responses to glucagon (200 ng/kg per min) were slightly lower in our patients with BEH than in control subjects and were not suppressed by propranolol. The data are compatible with a hyperreactivity of the beta-adrenergic receptors or of the adenylate cyclase or both in hyperkinetic BEH and could correspond to the previously observed exaggerated beta-adrenergic drive to the heart in this type of hypertension. The non-beta-receptor-mediated rise in plasma cAMP (glucagon), however, remains comparable in control subjects and BEH.

Adult↗
PubMed1976

Effects of beta-adrenergic blockade on plasma cyclic AMP and blood sugar responses to glucagon and isoproterenol in man.

In healthy humans glucagon infusion resulted in a significant increase in blood sugar and in plasma cyclic AMP. No discernible hemodynamic effects were found. Isoproterenol infusion on a mole per mole basis in the same subjects induced a significant, although less pronounced rise in plasma cyclic AMP, heart rate, and a fall in diastolic blood pressure but had no effect on blood sugar. Propranolol administration abolished the hemodynamic effects of isoproterenol and significantly decreased the response of plasma cyclic AMP; the same blocking dosage had little effect on plasma cyclic AMP changes induced by glucagon wheras the response in blood sugar was significantly reduced. These data in vivo are compatible with the in vitro demonstration of separate receptors for glucagon and isoproterenol.

Adult↗
PubMed1975

Pituitary responsiveness to gonadotrophin releasing factor (GnRH) in puerperium.

Administration of a single dose of Gondotrophin Releasing Factor (GnRF) failed to induce an increase in serum FSH immediately postpartum suggesting pituitary refractoriness. However, multiple injection of GnRF resulted in significant FSH increments but these were less than the FSH responses to a single injection of GnRF in normal menstruating women.

Female↗
PubMed1975

Labile (borderline) hypertension--new aspects of a common disorder.

Labile hypertension in patients under 50 years of age (the non-atherosclerotic form) was found to be characterized by higher urinary excretion of catecholamines and particularly of homovanillic acid; when further analyzed it was shown to be a heterogeneous entity with two types of patients clinically and biochemically distinguishable from each other, from control subjects and from patients with stable hypertension. Reactivity to assuming an upright posture distinguishes one type of labile hypertension having a normal postural pulse rate response from another having an excessive postural increase in pulse rate. The first group also showed normal responses of plasma norepinephrine concentration and of urinary cyclic AMP to posture. The group with excessive pulse rate response, in contrast, showed a decrease in plasma norepinephrine and an excessive increase of urinary cyclic AMP excretion in response to upright posture. The results suggest that not only circulating catecholamines but also the reactivity of their target tissues (as probably reflected by cyclic AMP measurements) are important in bringing about signs of adrenergic excess. The hypothesis that cyclic AMP changes reflect beta-adrenergic receptor reactivity is strongly favoured by data indicating qualitative differences in cyclic AMP responses to beta-adrenergic stimulation or inhibition between control subjects and those labile hypertensive patients with clinical signs of excessive sympathetic reactivity. The study stresses the need for more precise definition of labile hypertension, for dynamic clinical and biochemical correlative studies, and for consideration not only of the circulating hormones but also of the "second messengers" (such as cyclic AMP and cyclic GMP) which reflect the cellular action of hormones. Blood pressure is a very labile parameter in health and disease. In one sense, therefore, hypertension can be considered "labile" in every hypertensive patient. Usually, however, labile (or borderline) hypertension is regarded as characterized by a blood pressure over 140/90 mmHg, falling below these values with physical and emotional rest. This clinical entity, which affects some 20% (variously estimated between 16 and 30%) of the adult population, gives rise to uncertainties in both definition and prognosis. In some patients labile hypertension represents the precursor of a fixed hypertensive state, whereas in many others it remains labile throughout life, never progressing to the stable phase nor becoming associated with hypertensive cardiovascular disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Catecholamines↗
PubMed1975

Urinary and plasma cyclic adenosine 3',5'-monophosphate in patients with idiopathic edema.

Urinary excretion and plasma concentrations of adenosine 3',5'-monophosphate were determined in idiopathic edema patients both at rest and after assumption of the upright position. Patients and normal subjects responded similarly to upright posture with decreases in urinary volume and creatine excretion and their urinary excretion of cyclic AMP was not significantly different. The plasma concentration of cyclic AMP was high in patients, both in the recumbent and upright positions, and its renal clearance (unlike that of creatinine) was low. Plasma cyclic AMP increased in response to upright posture both in patients and normal subjects. Even if the significance of elevated plasma cyclic AMP is unknown, its presence without an increase in urinary cyclic AMP suggests that the renal handling of cyclic AMP is abnormal is idiopathic edema; this may be related to an excessive beta-adrenergic tone.

Adult↗
PubMed1975

Effects of morphine on serum growth hormone, cortisol, prolactin and thyroid stimulating hormone in man.

Morphine administration in man results in a significant increase in serum prolactin without altering the levels of growth hormone, thyroid stimulating hormone and cortisol. Apomorphine prevented the morphine induced prolactin rise. It is suggested that the effect on prolactin is not mediated via non specific stress or changes in the thyroid stimulating hormone releasing factor, but via suppression prolactin inhibiting factor or activation of a specific prolactin releasing factor.

Apomorphine↗
PubMed1975

Effect of clonidine on growth hormone, prolactin, luteinizing hormone, follicle-stimulating hormone, and thyroid-stimulating hormone in the serum of normal men.

Clonidine (0.15 mg iv), a selective noradrenergic receptor agonist, increased serum growth hormone (GH) levels (greater than 6 ng/ml) on 8 out of 12 administrations to 6 normal men. This increase was independent of the hypotensive effects of the drug and unrelated to changes in serum cortisol. Clonidine induced a hyperglycemic effect in all subjects which was greatest 15 min after commencint the injection. No changes in blood sugar or GH occurred after placebo injection. Apomorphine, a selective dopamine receptor agonist, elevated GH in each of these 6 subjects (greater than 10 ng/ml). Clonidine had no effect on serum prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), or thyroid-stimulating hormone (TSH). These data are compatible with a dual dopaminergic and noradrenergic mechanism modulating GH secretion in normal men and with the absence of a noradrenergic mechanism in the regulation of PRL, LH, FSH, or TSH.

Adult↗
PubMed1975

Dynamic evaluation of growth hormone (GH) and prolactin (hPRL) secretion in active acromegaly with high and low GH output.

Ten patients with active acromegaly were studied. In 9 plasma GH levels failed to suppress after glucose (OGTT), in 8 an increase in serum GH occurred after thyrotropin releasing hormone (TRH). After L-Dopa, 4 patients showed no change in serum GH, 3 exhibited a decrease and in 3 an increase in serum hGH occurred. With a combined insulin (ITT) and arginine (ATT) test, 2 patients exhibited an increase in hGH, and in 6 no change occurred. Fasting serum GH concentration was less than 11 ng/ml in 5 patients. Basal prolactin (hPRL) levels were normal in all patients including two with galactorrhea. L-Dopa suppressed and TRH stimulated hPRL secretion in all, but the responses which were seen were subnormal. Hydrocortisone infusion in two acromegalics did not affect the prolactin induced increase after TRH but blunted the GH increase after TRH.

Acromegaly↗