Adrenal glands of foetal sheep of 40 days gestation to term were incubated with and without ACTH or an increased [K+]. With ACTH, the 40 day foetal adrenal was capable of producing more cortisol and aldosterone per g body weight than was the term adrenal. ACTH was a potent stimulus to aldosterone and cortisol production in foetuses aged 60\p=n-\90days, and this effect declined significantly in the 91\p=n-\120day period. An increased [K+] was stimulatory to aldosterone production only after 120 days gestation. Peripheral blood levels of aldosterone, corticosterone, cortisol, 11-deoxycortisol and 11-deoxycorticosterone were measured in foetuses 60 days to term and the levels of aldosterone and cortisol were significantly lower in 90\p=n-\120day foetuses than in the younger or older ones. Direct adrenal vein cannulation proved all five steroids to be secretory products of the foetal adrenal.The ovine foetal cortex has been shown to play a significant role in the onset of parturition in this species (Liggins 1968) and for this reason its ability to

In spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, we examined tissue and adrenal norepinephrine concentrations, left ventricular (LV) weight, LV weight/body weight ratio (LV/BW), hlndquarter resistance properties, ie, perfusion pressures at maximum dilatation and constriction (PP^,, PPjni,,), and the slope of the methoxamine log dose-PP curve. In series 1, we studied 4-week-old controls (SHR C , WKYJ, sympathectomized rats (SX; SHR D , WKY D ), and SX rats also given prazosin (SXP; SHRnp, WKY,,,). With SX and SXP, adrenal norepinephrine concentrations increased in both strains, but tissue (LV, muscle, kidney) norepinephrine was depleted. At 4 weeks, LV/BW, PPmin, and PP MI were all greater in SHR C than in WKY C . With SX, these differences between strains remained unchanged, but SXP abolished them completely, indicating the importance of blockade of ar-adrenergic receptor stimuli of adrenal origin. In SHR C (but not in WKY C ), there was evidence of reinnervation after 4 weeks of SX. Hence, in series 2, the SXP period was extended to 8 weeks, and we studied SHR C , WKY C , SHR^, and WKY np . Systolic blood pressure was already elevated at 4 weeks in SHR C , and by 35 weeks it was 64 mm Hg greater than in WKY C . At 21 and 35 weeks, LV/BW, PP^,, PP B| ,, and slopes were all greater in SHR C than in WKY C , and the findings suggested greater LV and vascular hypertrophy than at 4 weeks. In SHR^ hypertension, LV hypertrophy and the vascular changes were completely prevented over the entire 35-week observation period. SXP mainly affected SHR and had few effects on WKY rats. The sympathetic nerves and adrenals are probably the sources of a-adrenergic receptor stimulation in young SHR. They account for the development of hypertension and for most of the cardiovascular structural differences between SHR and WKY rats. 12 This could be through increased resting neural activity, trophically induced cardiovascular hypertrophy, or both. Hypertrophy has usually been thought to occur as a consequence of the hypertension, 3 -5 but recent evidence in SHR suggests that it may precede the rise in blood pressure (BP), so that it could play a causal role in the development of hypertension.6 Hypertrophy contributes to the "amplifier" properties of the hypertensive circulation, whereby appropriate stimuli produce greater vascular narrowing and cardiac emptying. If the sympathetic nervous system were the major factor in initiating hypertension in SHR, then whatever the exact mechanism of action, adequate neonatal sympathectomy (SX) should prevent the rise in BP. In previous studies, hypertension has been attenuated by SX but not completely prevented.1011 It follows that other mechanisms are more important or that SX may have been inadequate. Originally, nerve growth factor antiserum (NGFA) was injected for several days after

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