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Biomedical subjects

J P Mtabaji

Publications and source records attributed to J P Mtabaji.

At least 19 recordsLinked to original sources
PubMed1993

Abnormalities in dihomo-gamma-linolenic acid release in the pathogenesis of hypertension.

Spontaneously hypertensive rats (SHR) respond to angiotensin and norepinephrine with an exaggerated pressor response. We have investigated the possibility that increased vascular reactivity in SHR may be related to a reduced synthesis of prostaglandin E1 (PGE1) resulting from a defect in the release of its precursor, dihomo-gamma-linoleic acid (DGLA). Isolated perfused mesenteric vascular beds of SHR and age matched Wistar-Kyoto rats (WKY) were perfused with Kreb's bicarbonate buffer. The effluent was collected and the fatty acid composition determined by gas chromatography. In SHR the release of DGLA, arachidonic acid, eicosapentaenoic acid, and virtually all other fatty acids detected in the effluent were reduced when compared to their normotensive controls. This difference could not be explained by low tissue fatty acid levels because these were higher in SHR. Evening primrose oil (EPO) when added to the diet increased the release of DGLA but not of other prostanoid precursors. EPO also reduced vascular reactivity and reduced blood pressure in SHR. It is suggested that the defect in the release of DGLA may be involved in the pathogenesis of hypertension because it occurs early before hypertension has actually occurred.

8,11,14-Eicosatrienoic Acid↗
PubMed1992

Ethnic differences in salt sensitivity: genetic or environmental factors?

1. The CARDIAC study, a world-wide cross-sectional epidemiological study on the relationship between alimentary factors and cardiovascular diseases, provided the initial evidence of ethnic differences in salt sensitivity; this was because despite much less urinary sodium excretion in Tanzania than in Brazil and the Japanese, the prevalence of hypertension was relatively higher in Tanzania than in the latter two populations. 2. To investigate this difference in salt sensitivity, a standardized clinical experiment was carried out: six to 13 male volunteers were placed on 2500 kcal basal diets containing 3 g salt/day. Eighteen grams of salt were added daily from the sixth to the 11th day in Tanzania and Brazil, while 22 g of salt were added in Japan. 3. Salt loading induced a significant rise in systolic blood pressure (SBP) on the second day of the high salt period (HSP) in Japan, the second and third day of HSP in Brazil, and all days of HSP in Tanzania. 4. Salt sensitivity was seen in 16.7% of the participants in Japan, 36.4% in Brazil and 46.2% in Tanzania. Further analysis of the effect of salt on blood pressure (BP) was carried out using the data from the CARDIAC study by multiple regression analysis. A within-centre comparison of fatty acid was also made. 5. The regression analysis revealed that the relationship of salt and blood pressure is more positively tight in Tanzania than Brazil and Japan after controlling for other confounding variables. Fatty acids in serum phospholipids contain significantly more palmitic acid and showed lower P/S ratios than those from Brazil and Japan.

Adult↗
PubMed1990

Diet and hypertension in Tanzania.

A survey was conducted on an urban population in the city of Dar es Salaam and on a rural community in both Handeni and the pastoral Masai in Monduli to investigate the relationship between diet and hypertension in Tanzania. Blood pressure (BP) was measured using an automatic BP-measuring machine. Biological markers of dietary intake were measured in 24-h urine and in blood. Hypertension was noted to be a bigger problem in the capital city, where the rate of obesity and salt intake were higher whereas potassium, protein, and polyunsaturated fatty acid intake were lower. Therefore, attention to dietary habits may reduce the growing problem of hypertension in Tanzania.

Adult↗
PubMed1990

The cardiac study in Tanzania: salt intake in the causation and treatment of hypertension.

The acute effects of varying salt intakes on the level of blood pressure in male normotensive volunteers in Tanzania were investigated. The subjects were kept on a diet supplying about 100 g protein, 85 g fat, and 2700 kcal per day. Daily potassium intake was about 50 mmol. The high salt diet increased urinary sodium excretion to 320 mmol/day while the low salt diet reduced sodium excretion to 52 mmol/day. Within 4-5 days there was a significant difference in mean arterial pressure between subjects on a high and a low salt diet. It is concluded that blood pressure in normotensive Tanzanian blacks is sensitive to alterations in salt intake. Although salt intake in Tanzania is relatively low, salt may be important in the causation of hypertension, and a reduction in salt intake may still have a place in the treatment and prevention of hypertension in Tanzania.

Blood Pressure↗
PubMed1988

Release of fatty acids by perfused vascular tissue in normotensive and hypertensive rats.

The release of fatty acids from perfused mesenteries of spontaneously hypertensive rats (SHR) and control Wistar-Kyoto rats (WKY) was studied. The release of the prostaglandin precursors dihomogammalinolenic acid, arachidonic acid, and eicosapentaenoic acid was reduced in SHR when compared with age-matched WKY. The release of all other fatty acids detected in the effluent was also reduced. The differences in fatty acid release were evident even when tissue levels of the fatty acids were similar or higher in SHR than in controls. The addition of evening primrose oil and fish oil into the diet partially corrected these defects. Evening primrose oil and fish oil both attenuated increases in blood pressure, but fish oil was more potent than primrose oil. Although both diets reduced vascular reactivity, primrose oil was more effective with lower doses of norepinephrine whereas fish oil blunted the effects of both low and high doses of norepinephrine. The possible mechanisms for the effects of primrose oil and fish oil on vascular reactivity are briefly discussed.

8,11,14-Eicosatrienoic Acid↗
PubMed1985

Zinc and vascular reactivity in rat mesenteric vessels: possible altered dihomo-gamma-linolenic acid metabolism in spontaneously hypertensive rats.

Zinc at a concentration of 0.4 microgram/ml potentiated pressor responses to norepinephrine in isolated perfused mesenteric vessels of SHR and WKY. At a higher concentration, 3.2 micrograms/ml, it inhibited responses to norepinephrine in WKY but produced no such inhibition in SHR. However, a transient potentiation was observed in SHR with the higher concentration. Pressor responses to potassium in WKY were not affected by zinc at either concentration. In SHR, however, the higher dose of zinc inhibited pressor responses to potassium. The low dose had no effect. Since effects of zinc may be mediated by release of DGLA, we suggest that in SHR DGLA release may be impaired.

8,11,14-Eicosatrienoic Acid↗
PubMed1985

The effects of indomethacin and PGE2 on vascular reactivity in spontaneously hypertensive rats: possible role of prostaglandins in the pathogenesis of hypertension.

Vascular reactivity was investigated in isolated perfused mesenteric vessels of young and adult SHR and age matched WKY. The primary objective was to investigate whether the difference in vascular reactivity between SHR and WKY would persist if endogenous prostaglandin synthesis was abolished and vascular reactivity restored with fixed exogenous quantities of PGE2. In young rats, when similar concentrations of PGE2 are infused in indomethacin blocked preparations, the difference in vascular reactivity between SHR and WKY is abolished. However, in adult rats the difference persists. It is concluded that enhanced prostaglandin synthesis in hypertension may participate in enhancing vascular reactivity.

Aging↗
PubMed1977

Actions of the tricyclic antidepressant clomipramine on responses to pressor agents. Interactions with prostaglandin E2.

Clomipramine inhibited pressor responses to potassium ions and vasopressin in the rat mesenteric vascular bed with an ID50 of about 1.8 microgram/ml against both pressor agents and the actions of indomethacin and PG2 on the clomipramine effect suggested that the drug may have been antagonising the action of an endogenous PG. This was supported by the inhibitory action of clomipramine on PG2 actions on guinea-pig ileum. A lower concentration also inhibited pressor responses to noradrenaline and angiotensin (ID50 about 9 ng/ml): inhibition was increased by PG2 and reduced by indomethacin. In this preparation potassium and vasopressin act primarily by stimulating calcium entry from the extracellular fluid whereas noradrenaline and angiotensin act primarily by releasing calcium from intracellular or membrane-bound stores. Our results can be explained by two actions: 1. a PG-antagonist action of clomipramine at the cell membrane and 2. a selectve inhibitory effect on release of intracellular calcium. Clomipramine may prove useful in studying PG and calcium-dependent mechanisms.

Angiotensin II↗
PubMed1977

Effects of prostaglandins on baseline pressure and responses to noradrenaline in a perfused rat mesenteric artery preparation. PGE1 as an antagonist of PGE2.

Concentrations of PGE1, PGE2, PGA1, PGA2 and PGF2alpha ranging from 10 to 10(5) pg/ml (2.8 x 10(-11) to 2.8 x 10(-7)M) were perfused through a rat mesenteric vascular bed preparation and their effects on baseline pressure and responses to noradrenaline noted. PGs A2 and FEalpha elevated baseline pressure at concentrations of 100 pg/ml and above but the other three PGs had little or no effect. PGs E2, A1 and F2alpha markedly potentiated responses to noradrenaline at all concentrations studied. In contrast PGs E1 and A2 caused a clear potentiation at 10 pg/ml but at higher concentrations the effect disappeared and concentrations of above 10(4) pg/ml were actually inhibitiory. E1 could antagonize the vascular effects of E2. These results offer possible explanations for some of the confusing findings reported in the literature.

Animals↗
PubMed1977

Prostaglandin A2 at low rates of infusion restores the antidiuretic effect of vasopressin in lithium-treated rats.

To test the effect of prostaglandin A2 (PGA2) on renal function, infusions of PGA2 (0-7 ng/kg/min), arginine-vasopressin (AVP) (1-25 ng/kg/min) and PGA2 plus AVP were administered to male rats made resistant to the antidiuretic effect of AVP by pre-treatment with lithium. In non-lithium-treated control rats, AVP had its expected antidiuretic action but in lithium-treated rats neither urinary volume nor osmolarity was changed. Prostaglandin A2 alone had no effect on urine output in lithium-treated rats; AVP plus PGA2 infused together evoked a near normal antidiuretic response. This antidiuretic action of PGA2 contrasts with the diuretic action reported by others. However, our infusion rates were 300-4000 times lower than those of other workers and it is suggested that PGs may have opposite actions on the kidney depending on their concentration. The effect of indomethacin (a blocker of prostaglandin synthesis) on urine flow was tested in five groups of rats on different régimes of liquid intake. Urine flow was reduced in the three groups with the highest urine volumes before treatment, and increased in the two groups with the lowest urinary volumes, again indicating that PGs may have both diuretic and antidiuretic actions.

Animals↗
PubMed1976

Vascular actions of frusemide and bumetanide on the rat superior mesenteric vascular bed: interactions with prostaglandins.

1. The addition of frusemide or bumetanide to perfusion fluid inhibited the response of the isolated mesenteric vascular bed to noradrenaline. 2. Addition of prostaglandin E2 to the perfusion fluid completely restored the response to noradrenaline. 3. Inhibition of prostaglandin secretion by indomethacin with restoration of responses to noradrenaline by the addition of exogenous prostaglandin E2 prevented the inhibitory effect of frusemide or bumetanide on responses to noradrenaline. 4. The inhibitory effects of diuretics on responsiveness to noradrenaline is mediated by blockade of endogenous prostaglandin synthesis.

Animals↗
PubMed1976

Vascular actions of furosemide and bumetanide on the rat superior mesenteric vascular bed: interactions with prolactin and prostaglandins.

The mesenteric vascular bed of the rat was used to investigate the effects of furosemide, bumetanide, prolactin, aspirin, indomethacin and prostaglandin E2 on the pressor response to norepinephrine. Furosemide, bumetanied and indomethacin could all inhibit the responses to norepinephrine: in each case responsiveness was restored by the addition of prostaglandin E2 to the perfusate. Bumetanide and furosemide both failed to inhibit responsiveness in the presence of an adequate amount (50 pg/ml) of prostaglandin E2. As has been shown previously, ovine prolactin in a concentration of 50 ng/ml enhanced pressor responses to norepinephrine while 500 ng/ml, after an initial potentiation, inhibited responsiveness. Aspirin, furosemide and bumetanide all reversed both the potentiation produced by the lower prolactin concentration and the inhibition produced by the higher one. When taken in conjunction with other evidence these results suggest that the diuretics exert their vascular effects by inhibiting prostaglandin synthesis whereas prolactin acts by stimulating such synthesis.

Animals↗
PubMed1976

Physiological cortisol levels block the inhibition of vascular reactivity produced by prolactin.

Cortisol in concentrations similar to the unbound levels of the hormone in human plasma can reverse the inhibition of vascular reactivity produced by prolactin. In the rat mesenteric vascular bed, cortisol alone in similar concentrations had no significant effect on the pressor responses to norepinephrine: the action of cortisol was seen only when prolactin was present. The relationships between the effects of different concentrations of prolactin and cortisol suggest that at some point there is a competitive interplay between the effects of the two hormones. There is indirect evidence that this interplay is at the level of prostaglandin synthesis or release. We suggest that cortisol has no effect on basal prostaglandin production but blocks the synthesis or release occurring in response to polypeptide hormone stimulation.

Animals↗