FACULTY OF BASIC MEDICAL SCIENCES
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Item Dietary salt and the glycaemic response to meals of different fibre content(The Macmillan Press Ltd., 1989) Akanji, A. O.; Charles-Davies, M. A.; Ezenwaka, C.; Abbiyesuku, F. A.; Osotimehin, B. O.In attempting to resolve the existing controversy on the effect of dietary salt intake on glycaemic responses, wc investigated post-prandial plasma glucose levels in 10 healthy normal weight non-diabetic Nigerian subjects (aged 23.1 years ± 1.3 (s.e.m.) with body mass index, BMI 19.9 ± 0.6kg/m2) consuming equal amounts of carbohydrate from glucose, boiled yam (tow fibre content of 0.9 per cent raw tuber weight) and boiled black-eyed peas (high fibre content of 4.8 per cent dry weight) with and without added table salt (4.25g). The results indicated no significant differences in fasting, peak and 2-h plasma glucose concentrations and total and incremental areas under the 3-h glucose/time curves in the subjects consuming each meal with and without added salt. Added salt had no influence on the glycaemic index of each meal. We conclude that salt has no effect on the glycaemic response to plain glucose or meals with varying fibre content even in a population known to demonstrate defects in salt handling.Item POST-JUNCTIONAL ALPHA ADRENOCEPTORS IN THE ANOCOCCYGEUS MUSCLE AND VAS DEFERENS: A COMPARATIVE STUDY IN NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS(1984-06) ADENEKAN, O. O.The characteristics of the post-junctional α-adrenoceptors in the isolated anococcygeus muscle and vas deferens were compared in spontaneously hypertensive rats (SHR) and normotensive rats (NCR). Responses to α —adrenoceptor agonists were obtained in the absence and presence of cocaine and of antagonists. Noradrenaline (NA) and phenylephrine (PE) produced concentration related contrations of the preparations which were antagonised by phentolamine, prazosin and yohimbine in both rat strains, indicating α -adrenoceptor mediation. The effects of cocaine revealed the relative efficiency of the uptake mechanism in each preparation. In the anococcygeus NA was equipotent in the NCR and SHR in the absence of cocaine whereas it was less potent in the SHR in the presence of cocaine, PE was less potent in the SHR in the absence and presence of cocaine. Antagonism was assessed by pA2 and K(diss) determinations. Potencies were compared only when antagonism was competitive in both strains. In the anococcygeus low concentrations of prazosin (L-Praz) non—competitively antagonised NA but antagonised PE equally and competitively in both strains. Higher concentrations (H-Praz) competitively antagonised NA in both strains. Phentolamine was competitive against NA in NCR and against PE in both strains. However, it was non-competitive against NA in SHR, Low concentrations of yohimbine (L—YOH) competitively antagonised NA and PE in both the NCR and SHR but the K(diss) values were significantly different. Higher concentrations (H—YOH) was competitive against NA in the NCR and PE in both strains. In the vas L-Praz competitively antagonised both NA and PE in the NCR but gave non—competitive antagonism of both strains in the SHR, Phentolamine antagonised NA competitively in the NCR but non-competitively in the SHR. It was equipotent and competitive against PE in both strains. L—YOH non-competitively antagonised NA and PE in the NCR but in the SHR it was competitive. H-YOH antagonism was non—competitive against both NA and PE in both strains. It is suggested that there might be both the α1— and α2 post—junctional adrenoceptor in the NCR anococcygeus muscle, Prazosin and yohimbine seem to be able to differentiate between the two receptor subtypes at low concentrations, It is suggested further that the α2- subpopulation might not possess identical characteristics in the NCR and SHR anococcygeus. Also, there might be an alteration in NA uptake properties in the SHR, In the NCR vas deferens there seems to be a predominance of post-junctional α1-adrenoceptors. In the SHR vas, there might be an increase in the post-junctional α-adrenoceptor population and/or sensitivity. Furthermore, it seems that the post—junctional α2-adrenoceptor characteristics are somewhat different in the SHR, Uptake1 is suggested to be less efficient in the SHR vas.Item INTERACTION OF PROSTAGLANDIN E(2) (PGE(2)) WITH NORADRENALINE AND ITS ANTAGONISTS IN THE ISOLATED MESENTERIC ARTERY OF RAT(1980-07) ADEAGBO, A. S. O.The effect of PGE(2), PGF(2a) and PGI(2) on constriction induced by different mechanisms was studied in the isolated rat mesenteric artery as described by McGregor (1965) Vasoconstriction was induced by mechanisms involving dif modes of calcium utilization viz: (i) Pharmacomechanical pathway by low doses of the adrenergic neurotransmitter, noradrenaline acting at α- receptor; (ii) electromechanical pathway by high potassium and (iii) agents which facilitate Ca(2t) influx e.g. A23187. The prostaglandins potentiated the vasoconstrictor effect of NA. Potentiation factors calculated from different doses of the prostaglandins showed the effects of the prostaglandins to be dose - dependent and PGE(2) to be significantly more potent (P>0.005) than PGF(2a) and PGI(2). The prostaglandins failed to potentiate high potassium - induced vasoconstriction. PGE(2) also failed to potentiate NA if the vasoconstrictor effects were evoked in Ca(2+) - free Krebs solution; but the degree of potentiation increased with increase in the concentration of Ca(2+) ions in the perfusion fluid. This result suggested strongly that the potentiation was associated with external calcium. Evidence is presented to show that potentiation was not prejunctional since cocaine, bretylium and reserpine pretreatment did not materially alter the effect of PGE(2). It was concluded that prostaglandins potentiated NA vasoconstriction by facilitating Ca(2a) influx. The mechanism of this facilitation is discussed. NA vasoconstriction was competitively antagonised by adrenoceptor antagonists-phentolamine, tolazoline, yohimbine and phenoxybenzamine (in low concentrations). The blockade caused by these antagonists was reversed by PGE(2). By comparing NA dose-ratios in the presence of antagonist with dose-ratios in the presence of antagonists plus different doses of PGB(2), I showed 1hat the degree of reversal was related to the dose of PGE. For example, the NA dose - ratio for yohimbine (1.28 x 10(-6)M) was reduced from 26.6 + 0.9 to 1.7 + 0.1 when PGE(2) (2.8 x 10(-8) M)was included in the perfusion fluid with the antagonist. The reverse of antagonism was not due to a change in the binding characteristics of the α- adrenoceptor since pA(2) values for the antagonist were not significantly different (P<0.05) when PGS was included with the antagonists. Evidence is presented which suggests that reversal of antagonism involved utilization of internally bound calcium since reversal of antagonism occured even after the omission of Ca(2+) from the external medium. In this sense, the mechanism of reversal was different from that of potentiation. Furthermore, the degree of reversal (measured as-reversal factor) was quantitatively greater than would be the case if reversal was simply a reflection of the enhgresponsiveness of the vascular muscle to NA. In contrast to the "competitive” α- adrenoceptor antagonists, PGE(2) did not reverse the block of NA vasoconstriction caused by phenoxybenzamine (high doses); verapamil, cinnarizine or prazosin. All these agents caused blockade of NA that was not competitive in nature. Since none of the competitive α- adrenoceptor antagonists prevent prostaglandin formation; the point is made, that a prostaglandin can reverse NA blockade even if the blockade did not involve inhibition of prostaglandin synthesis.