Growth hormone response to growth hormone-releasing hormone stimulation in oligozoospermic patients.

OBJECTIVE: To evaluate the GH response to growth hormone-releasing hormone (GH-RH) stimulation in oligozoospermic men. SETTING: Outpatient Clinic of Andrology at the Fundación Puigvert and the Department of Clinical Chemistry, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. PATIENTS: Fifteen oligozoospermic patients and 15 normozoospermic fertile men matched for age and body mass index. INTERVENTION: Endocrine status was determined by assay of basal levels of gonadotropins (FSH, LH), T, E2, inhibin, and insulin-like growth factor I (IGF-I). Serum GH levels were measured before and after GH-RH administration. RESULTS: GH response to GH-RH was significantly greater in patients than in controls. There was a positive correlation between the GH response and IGF-I levels in oligozoospermic patients only. Regression analysis showed a significant negative association of GH peak with inhibin after controlling for IGF-I in oligozoospermic patients. CONCLUSION: The results indicate that there is an altered responsiveness of pituitary to GH-RH administration in oligozoospermic patients; this did not appear to be due to the influence of gonadal steroid levels but rather to inhibin or some related peptide.

[Relationship of the renin-angiotensin-aldosterone system with auricular natriuretic factor in its response to the action of thiazide diuretics and to nifedipine, a sustained-release calcium antagonist]. / Relaciones del sistema renina-angiotensina-aldosterona con el factor natriurético auricular en su respuesta a la acción de diuréticos-tiacídicos y al antagonista del calcio nifedipino de liberación sostenida.

BACKGROUND: Blood pressure (BP) response to diuretics may be considered as an index of salt-sensitivity. Salt-sensitive patients may have an enhanced response to calcium channel blockers. In this study we correlate the basal values of two of the hormonal systems involved in the control of Na balance comparing them with the antihypertensive effects of a calcium channel blocker and a diuretic, to assess if BP response depends of a particular hormonal pattern by which we could define salt-sensitive patients. METHODS: We studied 21 essential hypertensive patients in a lineal sequence in an open protocol, first treated with slow release nifedipine (Nif-30), 30 mg daily, as a single dose, for 30 days, followed by amiloride+hydrochlorothiazide (HCT+Am), 50 mg and 5 mg, daily, for another month. Plasma renin activity (PRA), plasma aldosterone (PAld) and 24 hours urinary aldosterone (UAld) and atrial natriuretic factor (ANF), were measured at the start and end of the study. The hormonal values on each group were compared and correlated with changes observed in BP at the end of each period of treatment. RESULTS: HCT+Am decreased median arterial pressure (MAP) from 121.4 +/- 11 to 110.4 +/- 8 mmHg and Nif-30 to 108.7 +/- 12.4 mmHg, both p < 0.0004. There were 76% controlling MAP with Nif-30 whereas 48% did so with HCT+Am, p < 0.01, HCT+Am also increased PRA, PAld and decreased ANF, Ca urinary excretion and plasma PTH. Nif-30 did not alter the renin-angiotensin-aldosterone system, nor ANF. PTH remained unchanged. The MAP decrement caused by HCT+Am depended on baseline BP, r = -0.69, p < 0.0005, whereas Nif-30 decreased MAP independent from its baseline values, r = -0.02, NS. PAld showed a reverse correlation with ANF after treatment, r = -0.43, p < 0.05. The decrease of MAP holds a reverse relationship with ANF, both with HCT+Am, r = -0.47, p < 0.02, and with Nif-30, r = -0.45, p < 0.04. CONCLUSIONS: Treatment with Nif-30 was superior to HCT+Am in number of patients controlled, but the decrease in MAP is similar. Since the antihypertensive response to diuretic therapy and to calcium channel-blockers is related to low levels of ANF this fact could indicate some sort of defect of ANF secretion.

Small kidney and hypertension: selection of patients for surgery.

We studied 37 patients with various degrees of hypertension and a small unilateral kidney. Renal vein renin studies were shown to be positive on 19 occasions and negative on 18. Of those positive, 10 had severe and 1 moderate hypertension. Surgery cured 63.3%. In 27% blood pressure improved and 1 patient failed to respond. Eight patients had mild hypertension with a positive renal vein renin ratio (RVRR), but on observation their home blood pressures were normal without medication and they were not considered for surgery. Eighteen patients with mild hypertension and negative RVRR were also not operated. We believe that RVRR is important for a surgical decision, but only in severe and moderate hypertensives. In mild hypertension, measurement of blood pressure at home is normal on most occasions. These are hyperreactive patients and should not have surgery, regardless of the results of their RVRRs.

Renal tuberculosis and hypertension: value of the renal vein renin ratio.

We applied the central renal vein renin ratios in a group of patients with unilateral renal tuberculosis and hypertension to see whether the diseased kidney was involved in the pathogenesis of the elevated blood pressure. Of 20 patients 11 were nephrectomized, 7 had positive renal vein renin ratios and normal peripheral plasma renin activity; only 2 kept their blood pressure in control without medication. From 5 without a positive index, only 1 kept his blood pressure in control without medicine 1 year after surgery. The renal vein renin ratio has to be interpreted in light of other parameters, such as blood pressure, peripheral renin--if high the more the chance of being significant--and global renal function. The renal vein renin ratio alone per se gives poor information on the pressor role of a unilateral tuberculous kidney.

Plasma concentrations of ethynyl oestradiol and norethindrone after oral administration to women.

Plasma concentrations of ethynyl oestradiol and norethindrone in women were measured by radioimmunoassays after oral administration of 50 microng and 1000 microng respectively. The maximum values were obtained 1 h after administration. The calculated half-life was 6 1/2 h for ethynyl oestradiol and 7 h for norethindrone. At most 2-3% of the administered dose was present in the plasma at 1 h and had decreased to about 0-5% by 24 h.

Radioimmunoassay of norethindrone (17 alpha-ethynyl-17 beta-hydroxy-4-estren-3-one) and ethynyl-estradiol (17 alpha-ethynyl-1,3,5, (10)-estratien-3, 17 beta-diol). Application to human plasma determination of norethindrone after oral administration of this steroid.

The experiment conditions for the evaluation of Norethindrone (17 alpha-Ethynyl-17 beta-hydroxy-4-estren-3-one, NET) and Ethynyl-estradiol (17 alpha-ethynyl-1, 3, 5 (10) estratrien-3, 17 beta-diol, EE) by radioimmunoassay are described. A minimal quantity of 25 pg of these two steroids could be evaluated using different reduced metabolites of NET, very little cross reaction is observed with 200 pg of these metabolites. No effect was observed with estradiol for the EE-antiserum. The NET-antiserum was used to evaluate this steroid and ethynodiol diacetate after oral administration to female volunteers. Maximal values in the plasma (2-3% of the administered dose) was found between 1-3 h after administration and at 24 h a concentration of 0.1-0.3% still remained in the plasma.

PIP: The experimental conditions for the measurement of norethindrone (NET) and ethinyl estradiol (EE) in human plasma by radioimmunoassay are described. 25 pg of NET or EE could be detected by utilizing reduced me tabolites of NET. Minimal cross reaction occurred with 200 pg of the reduced metabolites. There was no apparent effect of estradiol for the EE antiserum. NET and ethynodiol diacetate were evaluated by the NET antiserum. Maximum plasma values (2-3% of the dose) of the compounds were observed 1-3 hours after administration. At 24 hours, the concentrations of the steroids in plasma was .1-.3% of the administered dose.