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Biomedical subjects

A L Mark

Publications and source records attributed to A L Mark.

204 records · Page 12Linked to original sources
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Augmentation of cardiopulmonary baroreflex control of forearm vascular resistance in borderline hypertension.

Arterial baroreflex control of heart rate is impaired in young men with borderline or mild hypertension. Despite this impairment, these subjects often have exaggerated increases in vascular resistance during orthostatic stress. We considered the possibility that this exaggerated reflex vasoconstriction might reflect augmented cardiopulmonary baroreflex control of vascular resistance in borderline hypertension (BHT). Accordingly, we studied cardiopulmonary baroreflex control of forearm vascular resistance in nine BHT men with blood pressure intermittently above 150/90 mm Hg and in seven normotensive (NT) men. Cardiopulmonary baroreceptor input was reduced with lower body negative pressure (LBNP-5 to-20 mm HG), which decreases cardiac filling pressures. Baseline mean arterial pressure was 99 /+- 3 mm Hg (mean /+- SE) in BHT vs 83 /+- 2 mm Hg in NT (p less than 0.05). Baseline forearm resistance was also higher in BHT than in NT: 19 /+- 2 vs 13 /+-1 mm Hg/ml/min/100 ml or units (p less than 0.05). Reflex increases in forearm resistance during LBNP were greater (p less than 0.05) in BHT than in NT 8.6 /+- 1.7 vs 4.5 /+- 1.1 units during LBNP-20). Increases in arterial pressure and forearm resistance during a cold pressor test were not significantly different in the two groups. Thus, the augmented response to LBNP could not be attributed to a nonspecific influence of increased baseline resistance or a generalized abnormality in reflex control. In summary, the results of this study suggest that there is augmentation of the tonic inhibitory influence of cardiopulmonary baroreceptors in humans with BHT.

Adult↗
PubMedDate not supplied

Structural changes in resistance and capacitance vessels in borderline hypertension.

Vascular resistance at rest may be normal in humans with borderline or mild hypertension. However, this finding is a facade which can obscure the presence of vascular structural alterations that may have an important influence on resistance and capacitance functions of the circulation. This paper reviews several studies regarding vascular structural changes in borderline hypertension (BHT). First, forearm vasodilator capacity is limited in BHT and in normotensive young men with a family history of hypertension; this suggests the presence of structural changes in forearm resistance vessels. Second, forearm venous distensibility is decreased in BHT. Most of this decrease is caused by nonadrenergic mechanisms--which suggests that there may be structural changes in veins in BHT. Third, the studies of Takeshita and colleagues suggest that sodium intake may influence vascular structural changes. In hypertensive patients who responded to salt loading with increased blood pressure and vascular resistance, salt loading limited vasodilator responses to 10 minutes of ischemia. This effect of salt loading on vasodilator responses occurred in some patients (salt-responders), but not in others (salt-nonresponders). Functional studies support the concept that structural changes in resistance and capacitance vessels occur during the early stages of human hypertension. These changes may not be entirely adaptive responses to elevated arterial pressure, since they occur in capacitance as well as resistance vessels. In addition, the structural changes appear to be responsive to factors such as sodium intake. These observations suggest that vascular structural changes in human hypertension may be related in part to neurohumoral influences or to primary vascular abnormalities.

Blood Vessels↗
PubMedDate not supplied

Factors that influence stroke in Dahl salt-sensitive rats.

Japanese rat chow and cerebral sympathetic denervation increase the incidence of stroke in stroke-prone spontaneously hypertensive rats. The purpose of this study was to determine if Japanese rat chow and sympathetic denervation would result in a high incidence of stroke in Dahl salt-sensitive (DS) rats, which have not been reported to be stroke prone. At 3 to 4 weeks of age, DS rats of both sexes began consumption of a high salt Japanese or American chow and underwent unilateral superior cervical sympathetic ganglionectomy. The rats fed American chow were found to have a high incidence of stroke (46%). Rats fed Japanese chow had shorter survival and a higher incidence of stroke (78%) than rats fed American chow (p less than 0.05). Blood pressure increased faster in DS rats fed Japanese chow (p less than 0.05). Metabolic studies indicated that increased sodium consumption accounted for only part of the acceleration of hypertension by Japanese rat chow. In DS rats grouped for equal levels of blood pressure, those fed Japanese chow had modestly reduced survival (p less than 0.05) compared with those fed American chow and had a greater incidence of stroke (85% vs 38%; p less than 0.05). Location of stroke was not influenced by removal of sympathetic nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Mechanisms of insulin action on sympathetic nerve activity.

Insulin resistance and hyperinsulinemia may contribute to the development of arterial hypertension. Although insulin may elevate arterial pressure, in part, through activation of the sympathetic nervous system, the sites and mechanisms of insulin-induced sympathetic excitation remain uncertain. While sympathoexcitation during insulin may be mediated by the baroreflex, or by modulation of norepinephrine release from sympathetic nerve endings, it has been shown repeatedly that insulin increases sympathetic outflow by actions on the central nervous system. Previous studies employing norepinephrine turnover have suggested that insulin causes sympathoexcitation by acting in the hypothalamus. Recent experiments from our laboratory involving direct measurements of regional sympathetic nerve activity have provided further evidence that insulin acts in the central nervous system. For example, administration of insulin into the third cerebralventricle increased lumbar but not renal or adrenal sympathetic nerve activity in normotensive rats. Interestingly, this pattern of regional sympathetic nerve responses to central neural administration of insulin is similar to that seen with systemic administration of insulin. Further, lesions of the anteroventral third ventricle hypothalamic (AV3V) region abolished increases in sympathetic activity to systemic administration of insulin with euglycemic clamp, suggesting that AV3V-related structures are critical for insulin-induced elevations in sympathetic outflow.

Animals↗