The functional orientation of vascular smooth muscle in the walls of aortae of DOCA-hypertensive and normotensive rats was determined by measuring the maximum force-generating capacity of strips cut at various angles from their aortae. The greatest tension produced by strips of aortae of either group was generated by strips cut perpendicular to the long axis of the artery. Strips of aortae from either group produced less tension if cut at different angles with respect to the circumferential axis. Cut at any angle, the strips of aorta from DOCA-hypertensive rats produced less tension than those from control rats at the same preload. In length-active stress studies, stress developed by strips cut from DOCA-hypertensive rats was less than that of control rats throughout the entire range of resting lengths. Stereologic analysis of histologic sections of aortae demonstrated a decrease in the volume fraction of smooth muscle in the media of aortic wall. No differences between the carotid arteries of the same DOCA-hypertensive and normotensive rats were found in the proportion of water (by weight) in their walls.

Levels of methionine-enkephalin immunoreactivity (MEI) and beta-endorphin immunoreactivity (BEI) were measured by means of a specific RIA in pituitary, hypothalamus, pancreas, and adrenal glands of db/db and control mice. We found significantly higher levels of MEI in the pituitaries of db/db mice than in either littermate or background strain controls. There was no significant difference in MEI levels in pancreas, adrenal glands, and hypothalamus. There was a significant difference in the BEI levels in the pituitaries of db/db mice compared with those in controls. No significant difference in BEI levels was observed between db/db and control mice in any of the other regions examined. We conclude from the above data that the opiate peptide system in the hypophyseal-hypothalamic axis of the db/db mouse is abnormal and warrants further investigation. The significance of this finding with respect to the possible etiology of diabetes mellitus is discussed.

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This study was done to delineate the role of alpha- and beta-adrenergic receptors and cyclic AMP in the mechanism of ethanol effects on insulin release from isolated islets. Rats were given an alpha-adrenergic blocker, phentolamine, or a beta-adrenergic blocker, propranolol. In addition, ethanol 1 g/kg was given intragastrically 1 h prior to sacrifice. Glucose mediated insulin release from isolated islets was enhanced by phentolamine and decreased by propranolol. Ethanol treatment inhibited glucose-induced insulin release from isolated islets of control rats as well as those given phentolamine and/or propranolol. Insulin release from isolated islets in response to dibutyryl-cyclic AMP was attenuated by ethanol. Theophylline enhanced glucose mediated insulin release from control islets but ethanol treatment produced a significant inhibition of insulin response. The data suggest that the site of action of the deleterious effects of ethanol on insulin release from isolated islets in rat does not involve adrenergic system and cyclic AMP.