Sympathetic supraspinal control of venous membrane potential in spontaneous hypertension in vivo.

To clarify the mechanisms controlling mesenteric venous membrane potential (Em) in spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY), Em was measured in vivo using flexibly mounted glass microelectrodes. Venous diameters were also measured. Ems under control conditions were significantly less in SHR. alpha-Adrenergic blockade with phenoxybenzamine (PBZ) significantly dilated and hyperpolarized SHR small veins but failed to alter the membrane potential of WKY small veins. After blockade with PBZ, membrane potentials were similar in both strains. Propranolol suffusion failed to alter the SHR membrane potential but depolarized WKY small veins. During blockade with PBZ, propranolol depolarized venous membranes equally in both strains. Membrane potentials after spinal section were similar in both strains and equal to the Ems during total adrenergic blockade. The data indicate that, in SHR, the relatively depolarized Em derives from altered alpha-adrenergic input. In SHR, alpha-adrenergic input appears to exert its depolarizing effect, at least in party, by interfering with the expression of endogenous, beta-adrenergic hyperpolarization. The beta-adrenergic influence, like the alpha-adrenergic input in SHR, is dependent on intact supraspinal pathways.

Method for chronic recording of electroencephalographic activity in conscious dogs.

The difficulties involved in recording high-quality electroencephalograms chronically from conscious dogs have been resolved by devising an implantable pure silver electrode assembly that can be screwed permanently into the skull. The assembly eliminates electromyographic artifacts and provides high-fidelity tracings. Construction is simple and commercially available, inexpensive parts are used. Highly satisfactory records can be obtained over periods of months.

Effects of angiotensin antagonists in various forms of experimental arterial hypertension.

The dependence of renal hypertension on increased levels of angiotensin II was investigated in conscious dogs at various stages of hypertension of four different types. Two of the most potent angiotensin inhibitors, Sar1-Ile8- and Sar1-Thr8-angiotensin II, were infused separately in various doses and at different times throughout the evolution of renal hypertension. The results of these experiments are consistent with the view that the renin-angiotensin system may participate in the acute and malignant phases of renal hypertension; they do not provide evidence for its participation when hypertension enters the chronic phase.