Bovine parathyroid extract and two commercial preparations containing the first 34 amino acids of synthetic bovine parathyroid hormone [bPTH41-34)] produced dose-related hypotension in anesthetized rats. Dogs were 10 times more sensitive to the two bPTH41-34) preparations than were rats.Propranolol, phentolamine, atropine, and promethazine did not affect the hypotensive action of bPTH-1-34) in rats and dogs. bPTH-1-34) decreased perfusion pressure in rat hindlimbs perfused in situ with Ringer's solution and was a vasodilator in dog kidneys perfused in vitro with Ringer's solution. Helical strips of rabbit aorta were also relaxed by bPTH41-34). We conclude that the direct vasodilatory action of bPTH preparations represents an intrinsic property of parathyroid hormone and that the hypotensive effect of this hormone is produced by part or all of the first NH2-terminal 34 amino acids.The antidiuretic action of exogenous parathyroid preparations in the South American lungfish (Lepidosiren paradoxa) was described in a previous report (1). Because renal function in lungfish is significantly affected by systemic blood pressure (2, 3), we suspected that the antidiuresis resulting from administration of parathyroid extracts might be related to a hypotensive action of this hormone. A vasodilatory action of parathyroid extract and the peptide containing the first 34 amino acids of synthetic bovine parathyroid hormone ] has been reported in dogs (4, 5). This hypotensive action of parathyroid hormone (PTH) has not been confirmed in any other vertebrate species. Furthermore, it was not clear whether the hormone is itself hypotensive or whether its action is mediated through other endogenous vasoactive substances.In a recent series of studies, we observed the vasodepressor actions of synthetic bPTH-(1-34) in the following vertebrates: the South American lungfish, the bullfrog, the water snake Natrix fasciata, and the domestic chicken (6). In the present studies we investigated the specific hypotensive actions of bPTH in the laboratory white rat and the mongrel dog. A dose-related vasodepressor response was demonstrated with two preparations of synthetic bPTH-(1-34). In both rats and dogs, the hypotensive action of bPTH-(1-34) was not inhibited by a-or 3-adrenergic, cholinergic, or histaminergic blocking agents. Furthermore, vasodilation could be demonstrated by using dog kidneys in vitro and rat hindlimbs perfused in situ with mammalian Ringer's solutions. Helical strips of rabbit aorta were also relaxed by bPTH-(1-34). On the basis of these results we propose that mammalian PTH has an intrinsic direct vasodilatory action on the vascular system. The exact mechanism of this action remains to be demonstrated. MATERIALS AND METHODSThree types of experiments were performed. Dogs and rats were used to determine the depressor effect of bPTH preparations in vivo. To test the vasodilatory effects of the synthetic bPTH-(1-34) in vitro, dog kidneys and rabbit aortic strips were perfused. In addition, rat hindlimbs were perfused ...

In the present study, responses to various agonists in thoracic aorta and tail artery strips, obtained from 4-week streptozotocin (STZ)-treated rats and age-matched controls, were studied. Responses in aorta obtained from diabetic animals to the alpha-agonists, norepinephrine (NE), and methoxamine (MOX), to calcium (Ca2+) and potassium (K+) were found to be depressed relative to control tissue. Responses in tail artery however, were found to be different. While responses to K+ were decreased and to Ca2+ unchanged, tail artery strips obtained from diabetic animals were found to be supersensitive to both alpha-agonists relative to control tissue. Another observed difference between the two tissues was in their catecholamine content. While induction of diabetes did not alter catecholamine levels in the aorta, a significant decrease was produced in the tail artery, relative to control tissue levels. Our results indicate that inherent differences (such as the degree of innervation) may contribute to the differential responses observed in the two tissues studied. They further suggest the possible involvement of alterations in calcium utilization in aorta and the development of postjunctional supersensitivity in tail artery obtained from STZ-treated animals.

To help address the clinical care gap, a working group discussed the future of faculty development in academic medicine, explored problems within the large, current enterprise devoted to continuing medical education (CME), and described four domains core to its revitalization and reformation. These domains are (1) preparing and supporting an engaged clinician-learner, (2) improving the quality of knowledge or evidence shared, (3) enhancing the means by which to disseminate and implement that knowledge and evidence, and (4) reforming the patient, health care, and regulatory systems in and for which the process of CME exists. Reshaping these domains requires the consideration of a more seamless, evidence-based, and patient-oriented continuum of medical education. Revitalizing CME also requires the full engagement of the academic medical community and its faculty. To achieve the goal of creating a new, more effective, seamless process of CME, the working group recommended an active faculty development process to develop strong clinician-learners, strong involvement of academic health center leaders, the development of an educational home for clinician-learners, and a meaningful national conversation on the subject of CME.