Michael G Collis

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We investigated vascular reactivity in isolated, Tyrode perfused kidneys from male (blood pressure, 222.6 mm Hg) and female (blood pressure, 178.5 mm Hg) spontaneously hypertensive rats (SHR, 4-6 months age) and sex and weight matched normotensive Kyoto Wistar and Wistar control rats. Optimal perfusion flows and basal pressures were similar in sex-matched(More)
1. Adenosine and its analogues relaxed the isolated rat aorta by an endothelium-dependent mechanism with an order of potency of 5'-N-ethylcarboxamidoadenosine (NECA) > 2-(p-(2-carboxy-ethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosi ne (CGS 21680) > adenosine = N6-(2-(4-amino-phenyl)ethyl)adenosine (APNEA) = N6-cyclopentyladenosine (CPA) >(More)
The numerous and widespread effects of adenosine provide both an opportunity for the development of novel therapeutic agents acting via adenosine receptors and the challenge of achieving selectivity of action. The feasibility of achieving selectivity is enhanced if receptor subtypes can be identified. Biochemical, functional and receptor-cloning studies are(More)
The purpose of this study was to determine whether the adenosine receptor that mediates relaxation of the noradrenaline-contracted guinea-pig aorta is of the A1 or A2 subtype. 5'-N-ethylcarboxamide adenosine (NECA) and 5'-N-cyclopropylcarboxamide adenosine (NCPCA) were about 100 times more potent as relaxants of the aorta than L-N6-phenylisopropyladenosine(More)
6-Cyclohexyl-N-hydroxy-3-(1,2,4-oxadiazol-5-yl)hexanamides were previously disclosed as inhibitors of procollagen C-proteinase (PCP) culminating in the identification of amide 1. Our objective was to discover a second inhibitor that would have improved affinity for PCP and to optimize properties for transepidermal delivery (TED) to intact skin. Further(More)
Receptors have been demonstrated on the terminations of the sympathetic adrenergic nerves. One type, the so-called alpha 2-receptors, are activated by the norepinephrine that is released from the nerve terminals into the synaptic cleft; this activation causes a reduction in the output of the transmitter (negative feedback). Recent studies have demonstrated(More)