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Biomedical subjects

T R Hansen

Publications and source records attributed to T R Hansen.

59 records · Page 4Linked to original sources
PubMed1980

Direct effect of phenylethylamine upon isolated rat aortic strip.

Phenylethylamine (PEA) has been implicated in a number of central and peripheral nervous system disorders. Its possible mechanisms of action include stimulation via catecholamine release and direct stimulation by PEA. We have examined the effects of PEA on isolated vascular smooth muscle (VSM) to further explore the mechanism by which PEA produces contraction in this tissue. Helical strips of rat aorta were suspended in a muscle bath. Smooth muscle contractions were recorded via force transducer. PEA elicited a concentration dependent contraction from these strips with a threshold near 10(-6) M and a maximum response at 5 X 10(-3) M. Pretreatment of rats with reserpine dramatically reduced the norepinephrine (NE) content of kidney, heart and spleen of these animals but did not prevent the action of PEA on VSM. The presence of phentolamine (10(-4) M) completely blocked the strip response to PEA. The presence of propranolol (10(-7) or 10(-4) M) altered but did not block the VSM response to PEA. These results argue that the effects of PEA upon the aortic strip preparation involve a direct action of this amine upon VSM.

Animals↗
PubMed1980

Orientation of arterial smooth muscle and strength of contraction of aortic strips from DOCA-hypertensive rats.

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.

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PubMed1975

Hypertension, transmural pressure, and vascular smooth muscle response in rats.

The effect of transmural pressure on the responsiveness of vascular smooth muscle was studied using rats with chronic occlusion of one external iliac artery. The arterial pressure in the occluded leg was reduced to approximately half of that in the contralateral unoccluded leg. Helical strips from the low- and high-pressure femoral arteries of spontaneously hypertensive rats and rats with deoxycorticosterone acetate-induced (DOCA) hypertension were compared with corresponding tissues from normotensive controls. The sensitivity of both low- and high-pressure artery strips from the spontaneously hypertensive rat was greater than that of controls when strontium or lanthanum was used as the agonist. The sensitivity of strips from both low- and high-pressure arteries from the DOCA-hypertensive rat was greater than that of controls when potassium, epinephrine, or calcium was the agonist. There was no difference in sensitivity between strips from the low- and high-pressure arteries in any group of rats. Maximum contractile force (contractility) was reduced in femoral artery strips from both legs of all hypertensive rats. The KCl-induced contraction of vascular smooth muscle from both femoral arteries of either form of hypertensive rat was not as readily depressed by high calcium concentrations as was that from the normotensive rat. Changes in sensitivity and contractility associated with hypertension could not be reversed by lowering blood pressure in one leg of a spontaneously hypertensive rat or prevented by protecting one leg from high pressure prior to the induction of DOCA hypertension. The altered sensitivity and contractility of arterial strips in these models of hypertension are not, then, secondary to the increase in wall stress.

Animals↗
PubMedDate not supplied

alpha 1-Adrenergic receptor binding in the spontaneously hypertensive rat.

Increased sympathetic outflow from the central nervous system to the periphery may contribute to the initiation of hypertension in spontaneously hypertensive rats (SHR). As this alteration in sympathetic activity may be mediated in part by alpha-adrenergic receptors in the central nervous system, the current study examined alpha 1-adrenergic receptors in various brain areas of SHR and normotensive Wistar-Kyoto control rats (WKY). The alpha 1-adrenergic receptor number and apparent affinity constants of brain sections of both young prehypertensive animals (4 weeks old) and mature hypertensive animals (12 weeks old) were studied with the alpha 1-adrenergic receptor antagonist [3H]WB-4101 to label the alpha-adrenergic receptor. Five brain regions were studied: rostral hypothalamus, caudal hypothalamus, locus ceruleus, nucleus tractus solitarius, and frontal cortical poles. In comparison to normotensive controls, mature hypertensive rats had a significantly greater density (p less than 0.05) of the alpha 1-adrenergic receptors in the rostral hypothalamus (+11%), caudal hypothalamus (+25%), and frontal cortical poles (+20%). Significantly greater (p less than 0.05) alpha 1-adrenergic receptor density was found in the rostral hypothalamus (+27%), caudal hypothalamus (+60%), and locus ceruleus (+39%) of the young prehypertensive SHR compared with age-matched WKY. These results indicate the presence of altered adrenergic receptor systems in the brains of genetically hypertensive animals and suggest that changes in the receptor systems take place during establishment of the hypertension.

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