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Biomedical subjects

I Os

Publications and source records attributed to I Os.

At least 91 records · Page 5Linked to original sources

Renal haemodynamic and sympathetic responses to head-up tilt in essential hypertension.

Nine mild-to-moderate hypertensive patients (HT), aged 41 +/- 0.6 years (mean +/- SEM) and nine age-matched normotensive control subjects (NT) were tilted to 60 degrees for 10 min. During tilt, both systolic (S) blood pressure (BP) (p less than 0.01) and diastolic (D) BP (p less than 0.05) increased in HT, but not in NT. At supine rest renal blood flow was higher in HT than in NT and increased by 17% in HT during tilt, while a decrease of 13% was observed in NT (p less than 0.05). Renal vascular resistance was unchanged in HT during tilt, while a significant increase (p less than 0.01) was observed in NT. Arterial plasma noradrenaline increased in both groups (p less than 0.05) during tilt, significantly more in HT than in NT (p less than 0.05). No statistically significant difference was observed between the groups in renal catecholamine uptake or release. Our data indicate enhanced general sympathetic and circulatory responses to tilt in subjects with mild-to-moderate essential hypertension. However, the enhanced haemodynamic and sympathetic responses were not shared by hypertensive kidneys and renovascular resistance remained unaffected by tilt.

Adult↗

General convulsions and rhabdomyolysis. Case reports.

Two patients who developed rhabdomyolysis secondary to generalized seizures are presented. Minor traumas of skeletal muscles due to seizures may be associated with myoglobinuria and the development of acute renal failure. The diagnosis rhabdomyolysis may easily be confirmed by following serum creatine kinase. Myoglobinuria is present if the urine turns dark brown with a heavily positive dipstick for urinary hemoglobin while microscopy of urinary sediment contains but a few red blood cells. Darkly pigmented granular urinary casts may also be present. In order to prevent development of acute renal failure, it is important to keep the diuresis high and alkaline. If renal failure develops it is usually reversible, but may necessitate peritoneal dialysis or hemodialysis for a couple of weeks.

Adult↗

Effect of dopamine and dopamine-antagonist infusion on blood platelet count, size and release reaction in hypertensive and normotensive subjects.

To examine the effect of dopamine on in vivo platelet function and a possible platelet contribution to the clearance of dopamine we measured platelet count, platelet size and plasma concentration of the platelet specific protein beta-thromboglobulin (BTG) in groups of 40 year old untreated hypertensive and normotensive men. One hypertensive (n = 10) and one normotensive (n = 10) group received dopamine infusion at doses from 0.5 to 2.0 micrograms/kg/min which increased plasma dopamine 100-fold from baseline. Two other groups of hypertensive (n = 10) and normotensive (n = 11) subjects received 10 mg of the dopamine antagonist metoclopramide intravenously, upon which serum prolactin concentration increased 10-fold. No significant effect on platelet function in any group was observed during these interventions. Platelet phenol-sulphotransferase may contribute to dopamine conjugation. However, the selected platelet parameters correlated only weakly with dopamine kinetics during the infusion. Neither dopamine nor a dopamine antagonist altered the selected platelet parameters, nor did these parameters influence the clearance of dopamine during a short-lasting pharmacological infusion.

Blood Platelets↗

Decreased serum phosphate in essential hypertension. Related to increased sympathetic tone.

Forty-year old men with untreated mild essential hypertension (n = 35) had decreased serum phosphate (P less than 0.001) concomitant with elevated resting plasma epinephrine (P less than 0.05) and heart rate (P less than 0.001) compared with age-matched, normotensive control men (n = 44). Blood pressure correlated negatively with serum phosphate (P less than 0.001) and positively with plasma epinephrine (P less than 0.01) and heart rate (P less than 0.01). Serum phosphate was significantly lowered during infusion of epinephrine, increasing arterial plasma epinephrine within the lower pathophysiological range corresponding to arousal reactions. Serum concentrations of immunoreactive parathyroid hormone were unchanged. Thus, hypophosphatemia in patients with mild essential hypertension appears to be inversely related to sympathetic adrenal tone and may be caused by increased plasma epinephrine within pathophysiologic arterial concentrations.

Adult↗

Increased platelet and vascular smooth muscle reactivity to low-dose adrenaline infusion in mild essential hypertension.

During low-dose adrenaline infusion, platelet count, platelet size, plasma beta-thromboglobulin (BTG) and forearm vascular resistance (FVR) were measured in twelve 40-year-old men with mild, untreated hypertension. The average platelet count increased from 195 to 226 X 10(9)/l (P less than 0.001), platelet size from 7.31 to 7.53 X 10(-15)/l (P less than 0.01), BTG from 0.61 to 1.08 nmol/l (P less than 0.02) and FVR decreased from 97 to 58 (arbitrary units; P less than 0.001) during the infusion. The change in platelet count reflects splenic release of platelets, the change in plasma BTG reflects platelet release reaction, while the reduced FVR reflects vascular smooth muscle cell relaxation. In 11 normotensive men aged 40 years, platelet count increased from 187 to 201 X 10 g/l (P less than 0.01) during an equal low-dose adrenaline infusion. This increase in platelet count is significantly less than in the hypertensive group (P less than 0.01). There was statistically no significant change in platelet size, BTG or FVR in the normotensive group. Arterial adrenaline rose from 0.5 to 2.5 nmol/l in the hypertensive and from 0.5 to 2.4 nmol/l in the normotensive group. A third group of 12 normotensive men received saline infusion: neither platelet parameters nor FVR changed in this group. Thus, a small and equal dose of adrenaline elicited a greater increase in platelet count, an enhanced platelet release reaction and a more pronounced forearm vasodilation in hypertensive than in normotensive subjects.

Adult↗

Hyper-responsiveness to low-dose epinephrine infusion in mild essential hypertension.

The present study was undertaken to evaluate the effects of intravenous infusion of small amounts of epinephrine on haemodynamics, renal electrolyte excretion and blood platelets in essential hypertension. Arterial plasma epinephrine concentrations were increased during the infusion to approximately 2.5 nmol/l both in a group of 40-year-old men with untreated mild essential hypertension (blood pressure 154 +/- 3/100 +/- 3 mmHg, n = 12) and in a group of age-matched male controls (124 +/- 3/78 +/- 2 mmHg, n = 11). In the hypertensive group only, mean blood pressure decreased, forearm blood flow increased, forearm vascular resistance decreased (P less than 0.001 for all) and the urinary excretion of sodium and potassium increased (P less than 0.01 for both). The hypertensive group also responded with an increase in plasma beta-thromboglobulin (P less than 0.05), blood platelet size (P less than 0.05) and a higher increase in platelet counts than in the normotensive group (P less than 0.05). Thus, in several ways the hypertensive patients showed a hyper-responsiveness to amounts of epinephrine which corresponds well to the plasma concentration achieved during psychological and physical activity.

Adult↗

Decreased central dopaminergic activity in essential hypertension.

Baseline serum prolactin (PRL) was found to be similar in 35 men with untreated essential hypertension (149 +/- 2/98 +/- 1 mmHg; means +/- s.e.) and 44 healthy normotensive men (126 +/- 1/80 +/- 1 mmHg), all 40 years old. A correlation between baseline PRL and aldosterone was found in the normotensive (r = 0.534, P less than 0.001), but not in the hypertensive group (r = -0.011, NS). Ten subjects from each group received intravenous metoclopramide, a competitive dopamine antagonist, while another 12 normotensive subjects were given saline only, and the effect on PRL, vasopressin (AVP) and catecholamines was followed. An exaggerated PRL response to metoclopramide was observed in the hypertensive group compared with the normotensive (P less than 0.05), and the mean normotensive peak value never exceeded the hypertensive. Plasma noradrenaline increased significantly compared with baseline (P less than 0.05) and the control group (P less than 0.001), concomitant with increased heart rate (P less than 0.05), after the administration of metoclopramide both in the hypertensive and normotensive group. After intravenous injection of metoclopramide, forearm blood flow increased significantly by 50% in the hypertensive (P less than 0.001), and 80% in the normotensive group (P less than 0.001) compared with the control group. Mean blood pressure remained unchanged as did plasma AVP, dopamine and adrenaline. The present study indicates an altered central dopaminergic activity in essential hypertension. Even at rest, endogenous dopamine exerts a modulating effect on noradrenaline release in both hypertensive and normotensive men.

Adult↗

Aging and urinary vasopressin excretion in healthy men.

The influence of age on urinary excretion of arginine vasopressin (antidiuretic hormone) was examined in three groups of healthy men, 25 +/- 1 (n = 12), 40 (n = 44) and 50 years of age (n = 28) respectively. Despite increasing plasma vasopressin with progressive age (2.5 +/- 0.6 vs. 3.5 +/- 0.4 vs. 7.4 +/- 1.0 ng/l, respectively) (means +/- SE), urinary excretion of vasopressin turned out similar (6.7 +/- 1.0 vs. 6.8 +/- 0.8 vs. 6.9 +/- 0.6 ng/h). No differences in sodium excretion, serum osmolality and creatinine clearance appeared that could explain these findings. The present results suggest that age-related impairment of renal concentrating capacity is compensated for by increasing circulating plasma vasopressin. Furthermore, differences in tubular handling of the hormone with age may explain the present findings, and may be another compensatory mechanism for decreased urinary concentrating ability.

Adult↗

Increased platelet size and release reaction in essential hypertension.

Basal platelet function was measured in 35 40-year-old men with untreated mild essential hypertension and compared with 44 age-matched normotensive men. The groups differed significantly with respect to platelet size in venous blood (hypertensive, 7.46 +/- 0.10 X 10(-15) l versus normotensive, 7.11 +/- 0.09 X 10(-15) l; P = 0.01) and arterial concentration of the platelet-specific protein beta-thromboglobulin (hypertensive, 1.11 +/- 0.23 nmol/l versus normotensive, 0.59 +/- 0.04 nmol/l; P = 0.02). The normotensive subjects had significantly higher beta-thromboglobulin (BTG) in venous than in arterial blood (P less than 0.01). The hypertensive men showed no such difference. In contrast to the normotensive subjects, the hypertensive group had reduced arterial compared with venous platelet count (P less than 0.01). This may reflect an increased liability in the hypertensive subjects to lose platelets through adherence to the cannula during arterial blood sampling. The above findings point to increased platelet activity in essential hypertension, particularly in arterial blood.

Adult↗

Endocrine and haemodynamic responses to graded dopamine infusion in essential hypertension.

Hormonal, mean arterial blood pressure, forearm blood flow and heart rate responses to graded dopamine infusion (0.5-2.0 micrograms/kg/min) were examined in 10 men with untreated essential hypertension WHO group I (147 +/- 4/100 +/- 1 mmHg, means +/- SE), and in 10 normotensive men (129 +/- 2/85 +/- 1 mmHg), all 40 years old. Another 12 normotensive men (126 +/- 3/80 +/- 2 mmHg) were given only saline infusion. Dopamine increased heart rate significantly in the hypertensive group (8 +/- 2 beats/min, p less than 0.001), but the heart rate remained unchanged in the normotensive group (1 +/- 1 beats/min, NS). Although dopamine infusion tended to decrease mean blood pressure, the changes were not significantly different from those observed in the control group. No change in forearm blood flow was observed in either group. In the groups given dopamine, prolactin levels decreased only slightly compared to the control group given saline, the decrement tending to be more pronounced in the hypertensive group. Plasma vasopressin remained unchanged in both groups during dopamine infusion. These results indicate that hypertensive patients exhibit increased sensitivity to the cardiovascular effects of dopamine.

Adult↗

The effect of sodium depletion and potassium supplementation on vasopressin, renin and catecholamines in hypertensive men.

Seventeen 50-year-old hypertensive men (157 +/- 4/110 +/- 2 mmHg, mean +/- SE) were given low sodium diet for one week, which was supplemented with potassium the following week. The urinary Na+/K+ excretion ratio changed from 2:1 to 1:5 and 1:12, respectively, during dietary intervention. Arterial plasma vasopressin decreased by 3.4 +/- 1.7 ng/l (0.05 less than p less than 0.10) and urinary excretion of vasopressin was reduced by nearly 50% (p less than 0.001) during sodium depletion, while plasma noradrenaline increased by 38% (p less than 0.001) and plasma dopamine showed an increase by 58% (p less than 0.001). Plasma renin concentration increased four-fold during sodium depletion (p less than 0.001). With combined salt depletion and potassium supplementation, arterial plasma vasopressin decreased by 9.5 +/- 4.0 ng/l (p less than 0.05) compared to control. Urinary excretion of vasopressin together with plasma noradrenaline and dopamine were unchanged during the second week. The reduction of blood pressure was most marked during the first week (143 +/- 3/103 +/- 2 mmHg, p less than 0.05), but continued to fall also during the second week. Thus, during sodium restriction in middle-aged hypertensive men, blood pressure reduction occurs concomitantly with inhibited vasopressin release, despite enhanced renin and catecholamine release. Potassium supplementation during sodium restriction induces only minor changes in these variables.

Blood Pressure↗

Hormonal responses to treatment of high blood pressure with low-salt diet alone and combined with added potassium.

One week strict sodium depletion in essential hypertensive men (n = 17) decreased blood pressure and body weight. Plasma renin concentration increased four-fold (p less than 0.001), plasma noradrenaline with 38% (p less than 0.001), plasma dopamine with 58% while plasma adrenaline remained unchanged. The urinary excretion of vasopressin was reduced with 50% (p less than 0.001). Extra potassium induced only small changes when already sodium depleted. Thus, vasopressin was the only pressor hormone which varied directly with sodium intake, blood pressure and body weight during sodium depletion.

Arginine Vasopressin↗

Central dopaminergic control of prolactin in essential hypertension.

An exaggerated, early prolactin response (p less than 0.01) was observed in ten patients with untreated essential hypertension (148 +/- 4/97 +/- 1 mmHg, means +/- SE) compared with ten healthy normotensive men of the same age (124 +/- 3/78 +/- 2 mmHg) after administration of metoclopramide, a competitive dopamine antagonist. The normotensive peak value of prolactin never exceeded that of the hypertensive (p less than 0.05). Since prolactin is considered an indicator of central dopaminergic activity, these findings suggest an altered central dopaminergic activity in mild essential hypertension.

Adult↗