Diabetes mellitus is increasing throughout the world. Cardiovascular disease (CVD) accounts for up to 80% of excess mortality in this high-risk population. Patients with diabetes have the same CVD risk factors as those people without diabetes. However, these risk factors are much more powerful in diabetic patients. CVD risk is especially high for diabetic women, and premenopausal diabetic women lose all the protection normally afforded to them by female sex hormones. Controlled clinical trials have clearly demonstrated that rigorous treatment of blood pressure, dyslipidemia and platelet hyperaggrebility strikingly reduces CVD risk in diabetic patients. Strategies directed at interrupting the renin-angiotensin system (both tissue and systemic systems) and the use of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors have proven to be especially beneficial for this high-risk population.

The immunoreactivity of a commercial preparation of human chorionic gonadotrophin (HCG) was determined in a homologous double antibody radioimmunoassay for HCG using antisera to the beta-subunit of the hormone. The immunoreactivity of the commercial HCG was found to be 2.2 +/- 0.3 (mean +/- 2 S.D.) times the biological potency. Exclusion chromatography of the commercial HCG and then curve resolution of the elution profile derived from the radioimmunoassay revealed that on a molar basis, 21% of the immunoreactivity was attributable to beta-HCG. The rate of clearance of this preparation of HCG from the plasma after intravenous administration was determined as a function of the dose administered to ten normal men (age 36--64 years). The doses ranged from 10,000 to 300,000 i.u. immunological potency. The rate of clearance decreased significantly (r = 0.574, P less than 0.05) with increasing doses of HCG from a mean of 786 ml/h at the lowest dose to a mean of 298 ml/h at the highest dose. The renal clearance of administered HCG also decreased with increasing doses; the mean renal clearance of the 10,000 i.u. dose was 3.6 times the mean renal clearance after administration of 200,000 i.u. When the accumulated urinary HCG was expressed as a percentage of the dose administered, 14.1% of the 10,000 i.u. dose and 9.8% of the higher doses accumulated in the urine, suggesting that non-renal clearance increased with increasing dose.

SUMMARY We have previously reported that 1) selective dietary sodium loading (without chloride) does not produce hypertension in rats of the Dahl salt-sensitive strain (DS) and 2) selective chloride loading (without sodium) lowers plasma renin activity in the intact Sprague-Dawley rat maintained on a low NaCI diet. The present study examined the effect of selective dietary chloride loading on two models of hypertension: the DS and the renin-dependent one-kidney, one clip Sprague-Dawley rat. The DS were pair-fed (n = 7/group) a "normal" NaCI, a high NaCI (4%), or a "normal" sodium-high chloride diet for 11 weeks. From Week 7 until the end of the experiment, the high NaCl-fed animals had higher (p ^ 0.05) blood pressures than animals fed either the normal NaCI or normal sodiumhigh chloride diet, which were not different from each other. Thus, in the DS, hypertension depends on high dietary intakes of both sodium and chloride. In one-kidney, one clip hypertensive rats, selective chloride loading failed to lower plasma renin activity (9 ± 1 vs 7 ± 1 ng angiotensin I/ml/hr) or to prevent hypertension (160 ± 10 vs 166 ± 9 mm Hg). Thus, selective dietary chloride loading (without sodium) does not alter blood pressure in either salt-sensitive or renin-dependent hypertension. (Hypertension 8: 56-61, 1986) KEY WORDS • Dahl salt-sensitive rat • sodium chloride • one-kidney, one clip hypertension E LEVATED arterial pressure is related to a high dietary NaCI intake in some hypertensive persons.' One animal model of salt-sensitive hypertension is the Dahl salt-sensitive rat strain (DS). Developed by Louis K. Dahl and colleagues, 2 DS are Sprague-Dawley rats inbred for their predisposition to become hypertensive on a high NaCI diet.2 For years, interest in salt-sensitive hypertension has focused primarily on the sodium ion. However, we have recently reported that selective sodium loading (without concomitant chloride) fails to produce hypertension in DS.3 -4 Similar observations have been described by Kurtz and Morris 5 and confirmed by us in another NaCl-dependent model of hypertension -the deoxycorticosterone acetate (DOCA)-salt treated rat. 6 In the present study, to further evaluate the importance of Received December 24, 1984; accepted June 12, 1985. chloride for NaCl-dependent hypertension, we compared the effects of dietary NaCI loading and selective chloride loading (without concomitant sodium) on blood pressure in DS. We have previously reported that inhibition of reniri release by NaCI in the intact Sprague-Dawley rat is specifically related to chloride.7 8 Thus, we hypothesized that, in the absence of sodium loading, selective chloride loading might inhibit renin release and hence lower blood pressure in a renin-dependent model of hypertension. To evaluate this hypothesis, we also studied the effects of selective chloride loading on plasma renin activity and blood pressure in NaCl-deprived Sprague-Dawley rats with one-kidney, one clip hypertension. In this model, elevated arterial pressure is renin-dependent r...

In an attempt to elucidate the mechanism of suppressive action of glucocorticoids on the hypothalamo-pituitary-ovarian axis, we studied the effects of short-term high dose dexamethasone administration of the LH and FSH responses to LHRH and to clomiphene in healthy women with normal menstrual cycles. Seven women, 21--35 years of age, received 100 micrograms of LHRH i.v. on day 6 of two consecutive menstrual cycles, once with and once without pre-treatment with dexamethasone 2 mg orally every 6 hrs. on days 2 through 5 of the menstrual cycle. Seven other women (ages 21--35 years) received clomiphene citrate 100 mg on days 2 through 5 of their menstrual cycle, once with and once without simultaneous administration of dexamethasone 2 mg orally every 6 h. The administration of dexamethasone suppressed baseline serum levels of LH and FSH and blunted LH and FSH response to both LHRH and clomiphene. The results indicate that short-term administration of pharmacological doses of glucocorticoids suppress the secretion of LH and FSH by a direct effect on the anterior pituitary and possibly by an effect at the hypothalamic level with inhibition of the release of LHRH.

We investigated exercise induced urinary albuminThe three groups did not differ in 24 h UAE. Exercise excretion rate (UAE) (ex-UAE) in patients with borderline induced a significant increase in UAE only in BH. Exerhypertension (

Non-insulin-dependent diabetic (NIDD) rats have an increased Ca2(+)-ATPase activity in their kidney basolateral membranes. We find that a similar increased activity occurs in erythrocytes of the NIDD animals. This alteration in membrane ATPase activity appears to be specific for the Ca2(+)-ATPase as (Na(+) + K+) and Mg2(+)-ATPase and Na, K and Mg concentrations in the erythrocyte were not affected by the diabetic condition in these animals. Thus, abnormalities in membrane Ca2(+)-ATPase activity in the NIDD rats are not restricted to one tissue and appear to be a generalized pathology in the NIDD animals.

The purpose of this study was to determine the effect of rendering newborn male Sprague-Dawley rats hypothyroid with ¹³¹I on development of the hypothalamic-pituitary axis. Hormonal responses to thyrotropin-releasing hormone (TRH). haloperidol (H), and luteinizing hormone-releasing hormone (LHRH) were determined at 9, 15, 30 and 75 days of age in hypothyroids and controls. Basal and TRH-stimulated thyroid-stimulating hormone (TSH) levels were higher in the hypothyroids, but the developmental patterns of basal TSH secretion and TSH reserve were parallel in the two groups, with maximal TSH secretion occurring at 30 days. Basal prolactin (PRL) and PRL responses to TRH and H were less in the hypothyroids at all ages. Basal LH and LH responses to LHRH were greater in the controls at days 9 and 15, but the hypothyroid rats displayed greater basal and stimulated LH secretion at 30 days and values similar to controls at 75 days of age. These results suggest that development of the hypothalamic-pituitary axis is altered in rats rendered hypothyroid shortly after birth.

Hypertension is often accompanied by a variety of metaabnormal more atherogenic LDL cholesterol particle. Dyslipidemia interacts with associated hemodynamic bolic abnormalities. These metabolic abnormalities include insulin resistance, dyslipidemia and abnormali-(ie, hypertension) and metabolic (ie, increased platelet aggregation and PAI-1 levels) in a multiplicative manner ties of the coagulation-fibrinolytic system predisposing to a procoagulent state. The nexus for all of these potentiating cardiovascular and renal disease. Accordingly, lipid therapy should be aggressive to attenuate abnormalities may be central (visceral) obesity. The dyslipidemia accompanying hypertension consists of low these medical complications of essential hypertension. HDL cholesterol, elevated triglyceride levels and an