Acute hypertension was induced in 19 anesthetized cats by the intravenous administration of angiotensin. The caliber of pial arteries was measured by a television image-splitting technique and local cerebral blood flow by the hydrogen clearance technique. As the blood pressure was increased, pail arterioles constricted and cerebral blood flow remained relatively constant, showing that autoregulation of cerebral blood flow was intact. At mean arterial pressures of more than 170 mm Hg arteriolar dilation appeared. In smaller arterioles (initial diameter less than 100 mum) a segmental dilation (the "sausage'string" phenomenon) frequently preceded uniform dilation. This arteriolar dilation was associated with a marked increase in local cerebral blood flow indicating that the upper level of autoregulation had been breached. In no cat was vasospasm or a decrease in blood flow observed during induced hypertension. Hypertension also caused dysfunction of the bloodbrain barrier since, in 17 out of 19 of the cats examined, there was extravasation of protein-bound Evans blue into brain tissue. In only one of the 19 cats subjected to neuropathological analysis was ischemic brain damage identified and this was restricted to minimal ischemic cell change. The results indicate that severe, induced hypertension in cats produces cerebral arteriolar dilation, an increase of cerebral blood flow, and dysfunction of the blood-brain barrier. These observations may be of importance in understanding the pathogenesis of hypertensive encephalopathy.

The US features of scrotal adrenal rests assist diagnosis of CAH.

(1) Hypertrophied SHR myocytes stimulated with action potentials had an increased calcium transient compared to normotensive cells. The greater calcium transient in the SHR cells is likely to be a major factor responsible for their increased contraction. (2) SHR myocytes had a prolonged action potential in comparison to normotensive cells. (3) The amplitude of ICa and myofilament response to calcium were unchanged in SHR myocytes, suggesting that these factors do not play a role in the increased contraction of these cells. (4) Since the difference between SHR and control cells was abolished by voltage clamping the cells to prevent the difference of action potential, it is unlikely that an alteration of intrinsic mechanisms in SHR myocytes is responsible for their increased contraction. Rather, it suggests that the prolonged action potential of SHR myocytes plays a important role in causing their increased calcium transient and contraction. Our results indicate that the prolonged action potential in SHR cells results in an increased calcium content of the sarcoplasmic reticulum, which leads to a greater sarcoplasmic reticular calcium release upon stimulation and an increased contraction.