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Biomedical subjects

J Atkinson

Publications and source records attributed to J Atkinson.

252 records · Page 14Linked to original sources

Disorderly conduct.

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Community Health Nursing

Business as usual.

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Health Services

Cyclohexamide and renin release following renal artery constriction.

Renal artery constriction in the uninephrectomized conscious rat produced "renin release": i.e. an increase in plasma renin level and a decrease in renal cortex renin level, and an increase in mean arterial pressure. A high dose (4 mg.kg-1) of the protein synthesis inhibitor, cyclohexamide, halved the rise in plasma renin level (with no change in renal cortex renin level and a fall in mean arterial pressure). We suggest that the increase in plasma renin level following renal artery constriction depends on (a) release from preformed renin stores and (b) de novo renin synthesis.

Animals

[Myoplasmic calcium-vasoconstriction coupling in the perfused caudal artery of adult spontaneously hypertensive rats. Effect of antihypertensive treatment].

In order to investigate whether smooth muscle intracellular calcium levels ([Ca2+]i) are related to hypertension and drug-induced changes in blood pressure, we studied basal perfusion resistance and basal [Ca2+]i and increases in perfusion pressure and [Ca2+]i using the fluorescent dye, fura-2 (dual wavelength excitation) in perfused tail artery. These were removed from 6 month old SHR previously treated (CAP + HCZ) for 10 weeks with captopril plus hydrochlorothiazide (44 and 22 mg/kg/day po, respectively). Separate groups received captopril (CAP) or hydrochlorothiazie (HCZ) alone, at similar doses, or no treatment (SHR). A fifth group of WKY normotensive rats did not receive any drug. Following determination of systolic arterial pressure (SAP) in awake rats, tail artery segments were removed and perfused at a constant flow rate with physiological salt solution plus fura-2/AM. Basal resistance and [Ca2+]i were determined. Then a dose-response curve for calcium chloride in the presence of a depolarizing concentration of potassium chloride was constructed. SAP was lowered in groups CAP + HCZ or CAP, but not in the group HCZ. Basal [Ca2+]i were similar in treated and untreated SHR and in WKY. Basal resistance to flow was lower in groups CAP + HCZ or CAP, and in WKY, than in untreated SHR. In depolarized arterial segments, vasconstrictor responses to perfusion with calcium chloride were lower in groups CAP + HCZ or CAP, and in WKY. Increases in [Ca2+]i were diminished in WKY rats. SAP measured in awake SHR and WKY was significantly correlated to basal and stimulated intracellular calcium-vasoreactivity coupling measured in vitro.

Animals