Search PubMed⌕ Search

Biomedical subjects

A L Mark

Publications and source records attributed to A L Mark.

At least 199 records · Page 11Linked to original sources
PubMed1972

The role of low pressure baroreceptors in reflex vasoconstrictor responses in man.

Studies were performed on 11 healthy men to evaluate the role of low pressure baroreceptors in the reflex forearm vasoconstrictor responses (plethysmography) to venous pooling produced by lower body negative pressure. Lower body negative pressure (LBNP) at - 5, - 10, - 20, and - 40 mm Hg lowered central venous pressure by 42, 59, 74, and 93%, respectively, and decreased forearm vascular conductance by 24, 29, 34, and 40%, respectively. The decreases in forearm blood flow and conductance during the low levels of venous pooling (LBNP - 5 and - 10 mm Hg) occurred without significant changes in arterial pressure, arterial dP/dt. and heart rate. These results with the low levels indicate that maneuvers which decrease venous return and central venous pressure in man can influence forearm vascular tone without significant changes in the determinants of carotid and aortic baroreceptor activity. During high levels of venous pooling (LBNP - 20 and - 40 mm Hg), significant decreases in arterial pressure and dP/dt and significant increases in heart rate accompanied the further reductions in central venous pressure, forearm blood flow, and forearm vascular conductance. About 73% of the decrease in conductance during venous pooling at LBNP - 40 mm Hg, which was sufficient to decrease arterial pressure and activate high pressure baroreceptor reflexes, occurred during low levels of venous pooling at LBNP - 10 mm Hg without changes in arterial pressure. This suggests that much of the forearm vasoconstriction with the high levels of venous pooling, which were sufficient to decrease arterial pressure, may be accounted for by reflexes originating in areas other than high pressure baroreceptors. The results of these studies suggest that low pressure baroreceptors exert an important influence on forearm vascular tone during decreases in venous return and central venous pressure in man.

Adult↗
PubMed1971

Responses of coronary vessels to adrenergic stimuli.

Coronary responses to adrenergic stimuli were determined in the intact beating heart before and after administration of practolol, 4-(2-hydroxy-3-isopropylaminoproproxy) acetanilide, which in low doses blocks myocardial but not vascular beta receptors. The left circumflex coronary artery of dogs was perfused with arterial blood at constant flow, and coronary perfusion pressure was measured. Before practolol, intracoronary injections of isoproterenol and norepinephrine and electrical stimulation of left cardiac sympathetic nerves caused reductions in perfusion pressure or vasodilatation associated with increases in left ventricular dp/dt, heart rate, and systolic pressure. After practolol, the coronary vasodilator response to isoproterenol was reduced by about 30% and occurred without significant changes in dp/dt, heart rate, and pressures. The addition of propranolol blocked completely the coronary responses to isoproterenol. Vascular responses to isoproterenol in the paw were not altered by practolol. Practolol antagonized the increases in dp/dt, heart rate, and systolic pressure and reversed coronary responses to norepinephrine and nerve stimulation from dilatation to constriction. The constriction, in turn, was reduced or reversed by phentolamine, an alpha receptor antagonist. Propranolol did not augment the constriction seen in response to norepinephrine and nerve stimulation after practolol. These results indicate that the coronary vasodilator action of norepinephrine and sympathetic nerve stimulation is indirect and caused by stimulation of myocardial beta receptors. The direct effect of these two stimuli on coronary vessels is minimal and is mediated through stimulation of alpha (vasoconstrictor) receptors. In contrast, the coronary vasodilator response to isoproterenol is both direct and indirect, resulting from stimulation of vascular and myocardial beta receptors; the direct vascular effect predominated in this study.

Adrenergic beta-Antagonists↗
PubMed1970

Responses of saphenous and mesenteric veins to administration of dopamine.

Others have observed that dopamine (3,4-dihydroxyphenylethylamine) constricts resistance vessels in skin, but dilates these vessels in the mesentery. We studied the effects of dopamine on cutaneous and mesenteric veins of dogs to see if this agent also produced qualitatively different effects on the tone of capacitance vessels (veins) in these vascular beds. The lateral saphenous or the left colic vein was perfused at constant flow with blood from a femoral artery. Pressures at the tip of the perfusion cannula and at the tip of a catheter 15 cm downstream were recorded continuously. Increases in the pressure gradient between these two points indicated venoconstriction; decreases indicated venodilatation. Dopamine and norepinephrine injected into the perfusion tubing caused constriction of both veins. The constriction was antagonized by blockade of alpha receptors. A dilator action of dopamine was not seen, even after alpha receptor blockade or in the presence of increased venous tone produced by serotonin, norepinephrine, or nerve stimulation. Reserpine and cocaine did not alter responses to dopamine in the saphenous vein; this suggests that the venoconstrictor action of dopamine results mainly from a direct effect on alpha receptors and that uptake into sympathetic nerve endings may not be important in regulating the amount of dopamine available to receptors in the saphenous vein.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Determinants of renal vascular resistance in the Dahl strain of genetically hypertensive rat.

Hypertension-resistant (R) rats of the Dahl strain remain normotensive on diets containing excessive sodium chloride, while hypertension-sensitive (S) rats rapidly become hypertensive when eating the same diet. In the present study, renal hemodynamics were investigated in Dahl rats eating normal or high salt chow for 4 weeks. The R rats eating sodium-enriched chow were found to have significantly lower renal vascular resistance (RVR) than R rats on normal chow; RVR was identical in S rats on either diet. The reason for the failure of S kidneys to exhibit vasodilation during high salt ingestion was explored by examining renal vascular responses to interruption of the renal sympathetic nerves, renal sympathetic nerve stimulation (SNS), and to several vasoactive agents. Changes in RVR to nerve section and to SNS were similar in both strains regardless of diet. Renal vascular responses to intraarterial norepinephrine were suppressed significantly by high salt intake only in the R rats. Changes in RVR to intraarterial angiotensin II were uniformly greater in S than in R rats, but were not altered by salt intake in either strain. Renal vasodilation in response to intraarterial acetylcholine was reduced in R rats on high salt intake, but was not affected by salt intake in S rats. It is concluded that S rats exhibit inappropriately high renal vascular tone during ingestion of excessive salt, and that this alteration is not the result of increased neurogenic activity or increased vascular reactivity to angiotensin II or norepinephrine.

Animals↗
PubMedDate not supplied

Does vasopressin contribute to salt-induced hypertension in the Dahl strain?

A humoral factor has been implicated in Dahl salt-sensitive genetically hypertensive rats. The goal of this study was to evaluate the pressor role of vasopressin (AVP) in Dahl rats. Salt-sensitive (S) and resistant (R) rats were fed either high (8%) or low (.04%) NaCl diets for 6 to 8 weeks. Blood pressure was elevated in S rats fed high salt diets (p less than 0.05). Plasma AVP increased with high salt diet in both groups (p less than 0.05), but was higher in S than R rats (2.0 +/- 0.3 and 1.3 +/- 0.2 microU/ml respectively, mean +/- SE, p less than 0.05). With low salt diet, plasma AVP did not differ significantly in S and R rats (1.0 +/- 0.2 and 0.7 +/- 0.2 microU/ml respectively). Pressor responses to intravenous injection of AVP were greater in S than R rats (p less than 0.05), but this difference was also observed with pressor responses to norepinephrine (S greater than R, p less than 0.05); there was no difference in pressor responses to AVP in S rats fed high vs low salt diet. Injection of 50 micrograms of d(CH2)5 VDAVP, which selectively inhibits vasoconstrictor effects of AVP, failed to lower blood pressure in S and R rats fed high or low salt diets despite the fact that this dose decreased pressor responses to 8 microU of AVP more than 90%. Although plasma AVP and vasopressor responses to AVP and NE are slightly elevated in S rats fed high salt, results with d(CH2)5 VDAVP suggest that vasoconstrictor effects of AVP do not play an important role in the maintenance of hypertension in Dahl S rats.

Animals↗
PubMedDate not supplied

Abnormal baroreflex control of heart rate in prehypertensive and hypertensive Dahl genetically salt-sensitive rats.

This study tested the hypothesis that in the Dahl model of genetic hypertension abnormal baroreflex function may precede and contribute to the development of hypertension. Sensitivity of baroreflex control of heart rate was assessed in conscious sensitive (S) and resistant (R) Dahl rats fed a high or low salt diet. Sensitivity of baroreflex control of heart rate was lower in S rats fed low salt although arterial pressure was not different from that of R rats. Hypertensive S rats showed resetting of baroreflexes to the higher pressure level without any further change in sensitivity. Pressor responses to phenylephrine were augmented in both prehypertensive and hypertensive S rats compared to R rats. Ganglionic blockade abolished this difference. In hypertensive S rats, ganglionic blockade decreased arterial pressure to levels not different than similarly treated R rats, indicating that neurogenic mechanisms contribute importantly to the early stages of hypertension in the Dahl model. These studies have identified impaired baroreflex function in prehypertensive and hypertensive Dahl S rats. This defect augments responses to pressor stimuli and may contribute to the development of salt-induced hypertension in the Dahl strain.

Animals↗