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Biomedical subjects

L F Obika

Publications and source records attributed to L F Obika.

At least 19 recordsLinked to original sources
PubMed1995

Pattern of paediatric blood pressure in rural, semi-urban and urban communities in Ilorin, Nigeria.

The blood pressures of 2,526 children aged between 1 and 14 years were measured in their home environments in rural, semi-urban and urban communities in Ilorin. Blood pressure increased with age, but there was no significant difference between the communities. Girls had higher blood pressures than boys between the ages of 9 and 13 years, in the semi-urban and rural communities. The prevalence of high blood pressure in the urban community (9.5%) was higher, though not significantly so, than the rural community (6.3%). It is concluded that the prevalence of paediatric high blood pressure in the African is higher than previously reported.

Adolescent↗
PubMed1993

Cardiovascular and catecholamine responses to acute haemorrhage in anaesthetized potassium-adapted rats.

The experiments were designed to determine whether potassium-loaded rats have a deficient recovery of blood pressure after a rapid arterial haemorrhage. Potassium loading was achieved by providing a 0.75% KCl solution as drinking fluid for 14 days, while control rats had either distilled water or tapwater. MAP, HR, Hct, and plasma electrolytes were determined before and after 1 and 2% body weight haemorrhage in anaesthetized Sprague-Dawley rats. Potassium-loaded rats had significantly reduced blood pressure recovery within 20 min after haemorrhage. HR was significantly reduced within 5 min only after 2% haemorrhage in potassium-adapted rats. Haemorrhage induced significant hyperkalaemia which was greater and significantly prolonged after 2% haemorrhage. The significant fall in Hct after haemorrhage was not affected by the magnitude of haemorrhage. In an additional group of rats, the pressor response to intravenous infusion of vasopressin was unaffected by potassium loading, whereas that to noradrenaline and angiotensin II was significantly reduced throughout the 20 min of infusion. The peak increase in blood pressure after phenylephrine injection was, however, unaffected by potassium loading. Basal plasma catecholamines concentration as well as concentrations after 1% haemorrhage were unaffected by potassium loading. It is concluded that the reduced vascular response to noradrenaline and angiotensin contributed to the reduced recovery of blood pressure after haemorrhage in potassium-loaded rats. Furthermore, the result with phenylephrine suggest a mechanism that is unrelated to direct vascular effects of noradrenaline and angiotensin II.

Acute Disease↗
PubMed1989

Haemodynamic responses to vasopressin in anaesthetized young and adult Brattleboro rats.

1. The cardiovascular effects of pressor doses of arginine vasopressin were examined in anaesthetized Brattleboro rats with hereditary diabetes insipidus (BDI) and normal rats of the parent Long Evans (LE) strain, either 37 or 85 days old. 2. Control mean arterial blood pressure and total peripheral resistance were similar in adult animals of the two strains but were significantly lower in the young BDI rats compared with the young LE rats. 3. The three doses of vasopressin produced greater pressor responses in the young, immature LE rats compared with the young BDI rats, whereas in the adult animals vasopressin had the greater pressor effect in the BDI rats compared with the LE rats of comparable age. 4. There was little effect of vasopressin on cardiac output after the initial decrease, particularly in the BDI rats whether immature or adult, despite more prolonged decreases in heart rate. 5. These studies indicate important age-related differences in the pressor response to vasopressin in anaesthetized rats, in addition to the clear differences in response between the animals with (LE) or without (BDI) the circulating endogenous peptide.

Aging↗
PubMed1989

Urinary kallikrein excretion during potassium chloride infusion in potassium-adapted rats: effect of amiloride.

1. Urinary kallikrein excretion in the anaesthetized rat was measured during intravenous KCl infusion in control and in K+-adapted rats. 2. The infusion of 0.1 mol/l KCl at 3.0 ml/h for 60 min in control rats resulted in a significant increase in urinary kallikrein excretion, associated with diuresis, natriuresis and kaliuresis. 3. When rats were offered 0.1 mol/l KCl to drink ad libitum for 14 days (K+-adaptation), the basal excretion of kallikrein was higher than in the control rats. In K+-adapted rats, intravenous infusion of 0.1 mol/l KCl resulted in significantly greater increase in urinary kallikrein excretion than in the control rats. 4. The Na+-channel blocker, amiloride (8.5 mg/kg body weight), significantly increased urinary kallikrein excretion immediately after injection in control and K+-adapted rats. However, in the subsequent 60 min, kallikrein excretion decreased markedly to values lower than those before injection of amiloride. 5. When amiloride was superimposed on a continuous 0.1 mol/l KCl infusion in K+-adapted rats, there was an immediate increase in kallikrein excretion. In the subsequent 20 min, kallikrein excretion decreased only to increase again in the next 40 min of KCl infusion. 6. Since amiloride injection reduces urinary kallikrein excretion in control and K+-adapted rats, the results suggest that urinary kallikrein excretion in the rat is through a mechanism(s) affected by amiloride. The high urinary kallikrein excretion and the greater response to KCl infusion in K+-adapted rats suggest that the K+-transport mechanism is more important than the mechanism affected by amiloride.

Amiloride↗
PubMed1989

Vasopressin V1-receptor blockade lowers arterial blood pressure in young conscious Long-Evans rats.

Young, conscious Long-Evans rats had significantly higher basal mean arterial blood pressure than age-matched Brattleboro rats with hereditary hypothalamic diabetes insipidus, and an intravenous injection of a specific vasopressin V1-receptor blocker significantly decreased the mean arterial pressure in the former animals only. The basal heart rate, which was significantly higher in the Brattleboro rats than in the Long-Evans rats, was unaffected by the vasopressin antagonist in either strain. These results indicate that vasopressin may be important in maintaining normal blood pressure in young rats.

Animals↗
PubMed1989

Effect of atrial natriuretic peptide on the release of rat renal kallikrein.

The effect of atrial natriuretic peptide (ANP) on renal kallikrein release was investigated in barbiturate anesthetized rats. ANP injections in a pharmacological dose (1 microgram i.v.) increased kallikrein excretion for about 15 min. The effect of ANP on kallikrein excretion was abolished when amiloride (2.5 mg i.v.) was administered prior to the injection of the peptide. Intravenous infusion of ANP (1 or 5 micrograms/h) or of isotonic saline (2 or 4 ml/h) did not alter urinary kallikrein output. When the ANP infusion was discontinued, the excretory rate of the enzyme tended to decrease. This decrease was prevented by the administration of 0.1 mg/h desoxycorticosterone-glucoside. A transient increase in kallikrein excretion, coincident with the appearance of diuresis, was observed during ANP infusion in the mineralocorticoid-treated animals. The rate of kallikrein release into the incubation medium by rat kidney slices was not affected by the presence of ANP (10(-9)M). These results can be interpreted as effects following an increased distal sodium delivery rather than a direct effect of ANP on connecting tubule cells (CNT cells).

Amiloride↗
PubMed1988

Effect of frusemide on urinary kallikrein excretion in the conscious rat: influence of adrenalectomy and DOCA treatment.

The effect of subcutaneous frusemide administration on urinary kallikrein excretion was studied in the conscious state, in control, adrenalectomized and DOCA-treated adrenalectomized rats. Frusemide increased urinary kallikrein excretion in the three groups of rats. Urine volume and urinary sodium and potassium excretions were also increased. These responses were however suppressed by adrenalectomy but normalized by DOCA treatment. It is concluded that frusemide's stimulation of urinary kallikrein excretion in the conscious rat is modulated by mineralocorticoid activity.

Adrenalectomy↗
PubMed1988

Transient hyperkalaemia immediately after acute haemorrhage in rats.

The effect of haemorrhage on plasma potassium concentration was studied in Sprague-Dawley rats, Brattleboro (BDI) rats and the parent strain Long-Evans (LE) rats. Haemorrhage induced an increase in plasma potassium within 10 min in all rats studied; 20 and 30 min later, plasma potassium was back to prehaemorrhage level. Changes in plasma sodium concentration were not statistically significant. When haemorrhage (1.0% of body weight) was repeated in the same animal preparation, there was a further significant increase in plasma potassium, but a fall in plasma sodium concentration. When vasopressin was injected intravenously, plasma potassium concentration did not change significantly (-0.21 +/- 0.21 mmol/l) in LE rats, whilst it increased significantly (0.69 +/- 0.20 mmol/l, p less than 0.001; paired t-test) in the BDI rats. The results suggest that haemorrhage-induced hyperkalaemia is unrelated to vasopressin, despite the fact that it increases plasma potassium concentration in the BDI rats when injected.

Animals↗
PubMed1988

Prolonged pressor responses to intravenously injected vasopressin in anaesthetized Brattleboro rats.

Randomized intravenous injections of arginine vasopressin, 0.02 to 0.62 micrograms/kg, administered to anaesthetized Brattleboro rats genetically lacking vasopressin, produced significantly greater, prolonged dose-dependent pressor responses than those produced in normal animals of the parent Long-Evans strain. Dose-related decreases in cardiac output were transient in both groups of animals but were greater in Brattleboro rats. It is concluded that the enhanced pressor effects in these animals were associated with greater and prolonged increases in the total peripheral resistance.

Animals↗
PubMed1987

Lack of pressor effect of dopamine in the pentobarbital-anesthetized rat.

The blood pressure and heart rate responses to intravenous dopamine infusion at 2.5, 5.0 and 10.0 micrograms.min-1 X 100 g-1 were studied in conscious and pentobarbital-anesthetized Sprague-Dawley rats. In the conscious rats, dopamine caused a significant dose-related increase in the mean arterial blood pressure which was abolished in the anesthetized rats. The heart rate increased significantly only at the highest dose infused. The responses to equipressor doses of noradrenaline (40 ng.min-1 X 100 g-1) and phenylephrine (1.0 micrograms.min-1 X 100 g-1) were also suppressed in the anesthetized rats. The results suggest that pentobarbital anesthesia depresses the blood pressure response to dopamine infusion in the rat through a depression of activation of alpha-adrenoceptors.

Anesthesia↗
PubMed1987

Amiloride inhibits the rise of urinary kallikrein excretion induced by frusemide administration in the rat.

The effect of amiloride administration on the urinary kallikrein response to the injection or continuous infusion of frusemide in normal Sprague-Dawley rats was investigated. Injections of frusemide induced repeatedly an increase in urinary kallikrein excretion. This effect was suppressed by amiloride. Amiloride also blocked the response to mannitol injection. A continuous infusion of frusemide lasting 100 min also induced an increase in urinary kallikrein excretion which persisted throughout the experiment. This response was completely blocked by the injection of amiloride. Urinary kallikrein excretion was directly and positively related to urine volume and urinary sodium excretion before and after amiloride injection. The regression lines had markedly decreased slopes after amiloride administration. The urinary kallikrein excretion was also positively related to the urine volume and urinary sodium excretion when frusemide was continuously infused. However, these relationships were abolished after amiloride injection. In both the injection and the infusion experiments, there was a direct relationship of urinary kallikrein excretion to urinary potassium excretion. Although this relationship persisted after amiloride injection, the regression line was shifted to the left. The suppression of the kallikrein stimulating effect of frusemide by the sodium channel blocker amiloride indicates that distal tubule sodium reabsorption is the triggering factor in urinary kallikrein excretion. The study suggests that the mechanism involved in the release of kallikrein by the distal tubular cells is linked to the renal mechanism affected by amiloride.

Amiloride↗
PubMed1987

Relationship of urinary kallikrein excretion to urinary potassium excretion during furosemide administration with and without amiloride.

The relationship of urinary kallikrein excretion to urine volume, and to urinary sodium and potassium excretions was studied in normal rats during furosemide diuresis and superimposed injection of amiloride, a K+-sparing diuretic. Continuous infusion of furosemide increased urinary kallikrein, sodium and potassium excretions and the urine volume. Amiloride injection during furosemide diuresis caused further increase in diuresis and natriuresis, but a prompt decrease in urinary kallikrein excretion to basal level, and potassium excretion to below the basal level. The significant correlation of urinary kallikrein excretion to urinary potassium excretion, but not to urine volume and urinary sodium excretion after amiloride injection suggests that the major determinant of urinary kallikrein excretion is renal potassium secretion through a mechanism that is affected by amiloride.

Amiloride↗
PubMed1987

Urinary kallikrein excretion after potassium adaptation in the rat.

24-h urinary kallikrein excretion in male Sprague-Dawley rats was measured before and after 14 days with 100 mM potassium chloride as drinking fluid ad libitum. Urinary kallikrein excretion increased in K+-adaptation. The increase was greater when the rats were given distilled water rather than 100 mM sodium chloride to drink prior to the potassium chloride. The urinary potassium excretion increased in all rats studied. The urinary sodium excretion, urine volume and fluid intake increased significantly in rats that had distilled water to drink prior to the KCl. In marked contrast, when rats were offered NaCl prior to KCl, the urinary sodium excretion was unaffected while the urine volume and fluid intake decreased significantly. This study shows that prior NaCl intake abolishes the natriuretic and diuretic effects of KCl load and only suppresses the increase in urinary kallikrein excretion. This suggests that K+ secretory activity at the distal tubules is the major determinant of the release of renal kallikrein in the rat.

Adaptation, Physiological↗
PubMed1986

Effect of bilateral nephrectomy on the recovery of blood pressure after acute hemorrhage in rats: role of renin-angiotensin system.

The effect of bilateral nephrectomy, and administration of an inhibitor of angiotensin converting enzyme, on the recovery of arterial blood pressure after hemorrhage (loss of 1% of b.wt), was studied in male Sprague-Dawley rats. Neither manoeuver significantly affected the recovery of blood pressure within the first 10 min after hemorrhage. Thereafter, the recovery of the blood pressure was markedly suppressed. The study suggests that the initial recovery of blood pressure is unrelated to the kidneys, but the later one requires their presence and depends on the activity of the renin-angiotensin system.

Animals↗
PubMed1986

Urinary kallikrein response to repeated frusemide injections in rats: effect of adrenalectomy and deoxycorticosterone acetate treatment.

The effect of repeated intravenous injections of frusemide (0.17 mg/kg) on the urinary kallikrein excretion of normal, adrenalectomized and deoxycorticosterone acetate (DOCA)-treated adrenalectomized rats was studied. Adrenalectomy decreased baseline urinary kallikrein excretion, while DOCA treatment restored it to normal. Frusemide injections repeatedly increased urinary kallikrein excretion in the three groups of rats studied. Compared with control and DOCA-treated animals, adrenalectomized rats were less responsive. The excretion of urinary kallikrein was positively correlated with urine volume and with the excretion of sodium and potassium in all groups. The regression lines were shifted to the left in DOCA-treated adrenalectomized rats showing that mineralocorticoids enhance the effect of frusemide on urinary kallikrein excretion. The regression lines between urinary kallikrein excretion and the measured variables in adrenalectomized rats did not differ from those of control animals. We conclude that the response of urinary kallikrein to frusemide is influenced by the level of mineralocorticoid activity. The effect of frusemide on urinary kallikrein excretion does not appear to be a 'wash-out' of the enzyme since its influence did not subside after repeated injections.

Adrenalectomy↗