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Biomedical subjects

D F Bohr

Publications and source records attributed to D F Bohr.

At least 109 records · Page 6Linked to original sources
PubMed1977

Structural and functional changes in vascular resistance and reactivity in the deoxycorticosterone acetate (DOCA)-hypertensive pig.

The development of altered vascular resistance and reactivity was characterized in a new model of hypertension, the deoxycorticosterone acetate (DOCA)-hypertensive pig. Terminal hindlimb perfusion studies were carried out on pigs (young uninephrectomized males) approximately 50 days after implantation of DOCA or control Silastic strips. Data from these studies showed that hypertensive vascular beds (n = 5) had significantly greater (P less than 0.005) resistances than controls (n = 9) both before and after maximla vasodilation with papaverine. In response to intra-arterial injections of norepinephrine, hypertensive pigs (n = 8) demonstrated shifts in the dose-response curves to the left and lower vasoconstrictor thresholds than controls (n = 10). Preliminary observations have been made on the effects of "protecting" the hindlimb vascular bed from the increased arterial pressure by external iliac artery ligation. Although this "protection" was incomplete it prevented the development of structurally based changes in resistance and reactivity, but did not prevent the development of increased vascular smooth muscle sensitivity. It is concluded that resistance vessels in the DOCA-hypertensive pig demonstrate changes in both structure and function; structural changes do not occur when the vessels are partially protected from the increased wall stress but this does not prevent the increase in sensitivity. The structural component of resistance makes a greater contribution to the overall increase in resistance in this stage of hypertension than does the smooth muscle contraction; however, since the structural change is secondary to the increase in arterial pressure, it cannot initiate the hypertension.

Animals↗
PubMed1976

Deoxycorticosterone hypertension in the pig.

1. Deoxycorticosterone acetate (DOCA) implantation (100 mg/kg) caused mean arterial pressure to rise in 5-10 days from control pressures of 100-115 mmHg to stable hypertensive values of 140-160 mmHg in approximately 1 month. In six of seven pigs elevations of mean arterial pressure were entirely the result of increased total peripheral resistance. 2. Single implants maintained serum DOCA at approximately ten times normal concentration for up to 90 days. 3. Moderate but variable decreases in serum aldosterone followed implantation. 4. Hypokalaemia, polydipsia and suppressed plasma renin activity were evident by the fifth post-implantation day and persisted thereafter. No consistent change occurred in serum sodium. 5. Noradrenaline or angiotensin caused increases in total peripheral resistance at lower threshold infusion rates in hypertensive pigs compared with control animals. 6. In isolated, perfused hind-limb preparations, hypertensive vascular beds were characterized by both functional (increased vascular smooth muscle sensitivity) and structural (elevated resistance of maximally dilated vascular bed) changes. 'Protection' from increased arterial wall stresses in hypertensive pigs prevented structural, but not functional, alterations.

Angiotensin II↗
PubMed1976

Relevance of vascular structural and smooth muscle sensitivity changes in hypertension.

This is a mini-review of the vascular changes that occur in experimental hypertension. Augmented vascular resistance and reactivity appear to be due to an increase both in wall thickness and in vascular smooth muscle sensitivity. The increase in wall thickness is an adaptive change that is secondary to the increase in arterial pressure; the altered smooth muscle sensitivity occurs in the absence of an increase in arterial pressure and hence may initiate the increase in vascular resistance and reactivity of experimental hypertension. Studies of subcellular function indicate that changes in smooth muscle sensitivity may be caused by an increase in cell membrane permeability and an altered handling of calcium by its subcellular sequestering system.

Animals↗
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↗
PubMed1975

Venous smooth muscle in hypertension. Enhanced contractility of portal veins from spontaneously hypertensive rats.

In isolated bath studies smooth muscle from the rat portal vein was evaluated for its reactivity and contractility, and the whole vessel wall was evaluated for its extensibility. Smooth muscle from the spontaneously hypertensive rat (SHR) had the following characteristics when compared with that from normotensive controls: (1) Spontaneous phasic contractions were more frequent and developed more tension; (2) threshold concentrations for responses to prostaglandins A-2 and B-2 were lower, but those for responses to epinephrine, norepinephrine, KCl, BaCl-2, and SrCl-2 were similar; (3) high concentrations of calcium had a less depressant action on the responses to the prostaglandins but not on the responses to the other agonists; (4) maximal contractile tensions to all agonists were greater; and (5) passive extensibility was less. These differences, because they are in the venous system, cannot be secondary to the increase in wall stress of arterial hypertension. The decreased passive extensibility in this vein in SHR creates a stiffer framework on which the active contractile process is able to develop greater tension. If this increase in active tension is generalized to all veins, it could be responsible for a decrease in venous capacity which increases the rate of venous return and, hence, increases cardiac output.

Animals↗