Biomedical subjects
D A Jenkins
Publications and source records attributed to D A Jenkins.
An inhibitory role for noradrenaline in the mouse vas deferens.
1 Noradrenaline (0.1-3.0 muM) inhibited the twitch responses to single pulse field stimulation of the isolated vas deferens of the mouse. The higher concentrations of noradrenaline (ca. 0.3-3.0 muM) were required to make the tissue contract.2 Phentolamine (10 muM) abolished the contractor response to higher concentrations of noradrenaline and antagonized the inhibitory effect of lower concentrations on the twitch response.3 Propranolol (10 muM) potentiated both the contractor and the inhibitory effect of noradrenaline on the twitch response.4 Isoprenaline (0.1-3.0 muM) and salbutamol (1.0-3.0 muM) both inhibited the twitch response. Their effects were antagonized by propranolol (10 muM), but not by practolol (10 muM).5 The effects of uptake(1) and uptake(2) blocking agents were determined. Cocaine (10 muM) reduced the size of the twitch response in 2 out of 4 experiments. Imipramine (0.18 muM) also reduced the size of the twitch, as did oestradiol (3.7 muM) and a combination of cocaine and oestradiol.6 Contractor responses to exogenous noradrenaline showed tachyphylaxis, but when this was not very marked, the response could be shown to be potentiated by uptake blocking agents.7 The inhibitory effect of noradrenaline on the twitch response was greatly potentiated by cocaine (10 muM) and much less so by oestradiol (3.7 muM).8 It is concluded that the transmitter responsible for the twitch response is either an unknown substance released from the sympathetic neurone, or noradrenaline acting upon a receptor with none of the characteristics of known alpha- or beta-adrenoceptors. In either case, noradrenaline can inhibit the output, probably by stimulation of presynaptic alpha-adrenoceptors.
Proceedings: Is noradrenaline the motor transmitter in the mouse vas deferens?
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Letter: Incidence of alcoholic liver disease.
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Proceedings: Is morphine inhibition to the twitch response of the mouse vas deferens mediated via noradrenaline?
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Calcareous sponge spicules: a study of magnesian calcites.
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Blood glucose control determines the renal haemodynamic response to angiotensin converting enzyme inhibition in type 1 diabetes.
Elevation of glomerular filtration rate (GFR) is a feature of diabetes mellitus in humans and in animal models. Angiotensin II has been implicated as a mediator of GFR in diabetes. The acute effect of inhibition of angiotensin converting enzyme with captopril on renal haemodynamic and endocrine parameters was therefore studied in 14 normotensive male Type 1 diabetic patients, and the responses compared with those in five normal male control subjects. Following captopril 12.5 mg orally the diabetic patients exhibited an acute fall in GFR from 122 +/- 3.8 to 113 +/- 4.5 ml min-1 1.73-m-2 (p less than 0.02) and a rise in renal plasma flow (RPF) from 670 +/- 57 to 797 +/- 46 ml min-1 1.73-m-2 (p less than 0.01) which resulted in a fall in filtration. This did not occur in normal control subjects. Natriuresis occurred only in normal control subjects. There was no change in urinary excretion of PGE2 or kallikrein in either group but excretion of 6-keto-PGF1 alpha fell in the diabetic patients. There was a significant correlation between glycosylated haemoglobin and baseline RPF (rs = -0.79, p less than 0.001) and filtration fraction (rs = 0.83, p less than 0.001) that persisted when the change in these variables following captopril was analysed. Our results are compatible with the response to ACE inhibition in diabetic patients being secondary to inhibition of angiotensin II and suggest that this response may be related to blood glucose control.
Transfer anxiety in patients with myocardial infarction.
When patients are transferred from a coronary care unit to a general ward they often experience transfer anxiety. A structured pre-transfer teaching programme is suggested as a tool which may improve patient care.
Effect of added fiber on the glucose and metabolic response to a mixed meal in normal and diabetic subjects.
10 g of guar was added to a test meal given to 11 subjects, six of whom had insulin-dependent diabetes, after an overnight fast. The addition of guar to the meal produced an overall decrease in the blood glucose concentrations after the meal in both normal and diabetic subjects. The insulin secretory response in the normal subjects was less when guar was included in the meal than when it was not. In normal subjects, but not in diabetic subjects, the addition of guar also resulted in a diminished response of lactate, pyruvate, and alanine to the test meal and a blunting of the fall in serum ketones. This is likely related to the fact that the same dose of insulin was given in the diabetic subjects with both test meals. Thus, in the normal circumstances, the diminished glycemic response to the guar-containing meal resulted in diminished insulin secretion, which was not the case with the diabetic subjects.