Pressor Dose Research Articles

SYMPATHETIC ACTIVITY AND PRESYNAPTIC ADRENOCEPTOR FUNCTION IN PATIENTS WITH LONGSTANDING ESSENTIAL HYPERTENSION

To assess the contribution of the sympathetic nervous system to the hypertension in patients with longstanding essential hypertension. Overall sympathetic function, presynaptic adrenoceptors and neuronal re-uptake were examined after withdrawal of medication for at least 3 weeks in eight patients with longstanding essential hypertension and in eight carefully matched normotensive control subjects. Minimal forearm vascular resistance after 10 min ischaemia was used as a measure of structural vascular changes. Overall sympathetic tone was assessed using tilt testing and pressor dose infusion of noradrenaline. The presence and function of presynaptic adrenoceptors and the neuronal re-uptake of noradrenaline were evaluated in the forearm using tracer noradrenaline kinetics with measurement of forearm noradrenaline plasma appearance rate and noradrenaline plasma spillover. Intra-arterial infusions of tritiated noradrenaline, the endogenous alpha- and beta-adrenoceptor agonist adrenaline, the alpha-adrenoceptor blocker phentolamine, the non-adrenergic vasodilator sodium nitroprusside and the neuronal re-uptake inhibitor desipramine were given in the forearm. We found that the hypertensives had higher minimal forearm vascular resistance, indicating structural vascular changes; decreased overall sympathetic activity, indicated by a lower basal whole-body noradrenaline production rate; enhanced vasopressor sensitivity for exogenously administered noradrenaline with decreased arterial baroreflex sensitivity; indications of decreased forearm neuronal re-uptake; evidence consistent with the presence of presynaptic, release-facilitating beta-adrenoceptors in the forearm, apparently not functionally different between the two groups; and undecisive evidence for the presence of functional presynaptic alpha-adrenoceptors in the forearm. In patients with longstanding essential hypertension we found decreased overall sympathetic activity, with indications of decreased forearm neuronal re-uptake, which might have a compensatory role. We found indications of structural vascular changes and diminished baroreflex sensitivity in the hypertensives, which contribute to the hypertension. However, peripheral presynaptic, release-facilitating beta-adrenoceptors seem to be present, which are functionally not clearly different between the two groups. Observations on peripheral presynaptic alpha-adrenoceptors were inconclusive.

143 The effects of pressor and subpressor doses of angiotensin II on insulin sensitivity

143 The effects of pressor and subpressor doses of angiotensin II on insulin sensitivity

The differential effects of circulating norepinephrine and neuronally released norepinephrine on sodium excretion in humans.

The renal effects of incremental infusions of norepinephrine (placebo, 0.025 mu/kg/min), 0.075 micrograms/kg/min, phenylephrine (placebo, 0.5 micrograms/kg/min, 2.5 micrograms/kg/min), and tyramine (placebo, 2 micrograms/kg/min, 15 micrograms/kg/min) were examined in three respective groups (n = 9, 8, and 8) of normotensive male subjects undergoing water diuresis. Tyramine is an indirect sympathetic agent that causes neuronal release of endogenous norepinephrine. Increases in mean arterial pressure during each high-dose infusion were comparable in all three groups. Both norepinephrine and phenylephrine caused a decrease in urinary sodium excretion and effective renal plasma flow, with no changes in glomerular filtration rate. Proximal tubular sodium reabsorption, as assessed by both lithium clearance and solute-free water clearance methods, was increased by pressor doses of norepinephrine and phenylephrine. In contrast, a similar pressor dose of tyramine was associated with a pressure natriuresis, an increase in effective renal plasma flow, and a decrease in proximal tubular sodium reabsorption. Our data indicate that, in normotensive humans, circulating catecholamines (norepinephrine and phenylephrine) have opposite effects on renal sodium handling from neuronally released norepinephrine (tyramine).

Cocaine potentiates the blood pressure and cerebral blood flow response to norepinephrine in rats

Acute drug-induced hypertension is known to have adverse consequences on the cerebral vasculature. Cocaine abuse has been reported to be associated with an increased frequency of hemorrhagic or ischemic stroke. The purpose of this study was to determine whether cocaine alters the blood pressure or cerebral blood flow response to exogenous norepinephrine. A craniectomy was made over the parietal cortex in rats and cortical blood flow changes were measured using laser-Doppler flowmetry. Ten minutes after cocaine (1 mg/kg, i.v.) or saline, increasing doses of norepinephrine (0.01–10 μg/kg, i.v.) were given by bolus injection and changes in blood pressure and flow were monitored. Cocaine produced a transient 27±5% increase in blood pressure and a 38±9% increase in blood flow. Cocaine significantly potentiated the blood pressure and cerebral blood flow responses produced by submaximal pressor doses of norepinephrine (0.01–0.6 μg/kg, i.v.). In summary, cocaine causes a rapid, transient increase in blood pressure and cortical blood flow and potentiates the magnitude and duration of the pressure and flow response to norepinephrine. Repetitive blood pressure elevations in cocaine abusers is one of the proposed mechanisms leading to damage of cerebral vessels. These results may be relevant to an increased frequency of cerebrovascular accidents in cocaine-abusing individuals.

Potential role of endothelin-1 in the pathogenesis of acute hypertensive vascular disease in the rat

Endothelin-1 (ET-1) is a potent and long-acting vasoactive peptide often implicated in the pathogenesis of hypertension. However, little is known about its role in the pathogenesis of hypertensive vascular disease. This study compares the vascular changes produced in vivo by pressor or subpressor doses of ET-1 and angiotensin II (ANG II) in rat intestinal arterioles. In one experiment, equivalent pressor doses of either ET-1 (0.2 μg/kg/min) or ANG II (2 μg/kg/min) were given. In a second experiment, subpressor doses of ET-1 (10 ng/kg/min) were either infused alone or given in combination with pressor doses of ANG II (2 μg/kg/min). Normal saline infusions (0.02 mL/min) served as controls. All infusions were continued for 60 minutes, interrupted for 30 minutes, and reinstituted for 30 minutes. Changes in vascular permeability were assessed using ferritin as a tracer; vascular lesions were assessed by computerized morphometry and electron microscopy. Results from the first experiment showed that ET-1 and ANG II produced approximately equivalent increases in blood pressure but that ET-1 had more prolonged pressor effects when infusions were interrupted. Pressor doses of either ET-1 or ANG II caused a segmental pattern of vasoconstriction and dilatation, an increase in ferritin permeability, and severe vascular smooth muscle damage. However, vessels from ET-1-treated animals had fewer damaged smooth muscle cells ( p < 0.05) and smaller areas of vessel wall damage ( p < 0.05) than did those from the ANG II-treated group. Subpressor doses of ET-1 in the second experiment produced no vascular lesions, but combined subpressor ET-1/pressor ANG II infusion caused greater hypertension ( p < 0.05) and more extensive damage ( p < 0.01) to greater numbers of vascular smooth muscle cells ( p < 0.01) than did pressor infusions of ET-1 or ANG II alone. The results indicate that subpressor concentrations of ET-1 clearly potentiate the vascular damage caused by ANG II-induced hypertension. On the other hand, pressor doses of ET-1 do not cause more severe vascular injury than do equipresor doses of ANG II, though the hypertension induced by ET-1 has longer-lasting hypertensive effects.

Pressor doses of angiotensin II increase insulin-mediated glucose uptake in normotensive men.

The effect of pressor doses of angiotensin II infused intravenously on insulin-mediated glucose uptake was determined in normotensive men. A 3-h hyperinsulinemic euglycemic clamp was employed in 14 normotensive subjects to determine insulin-mediated glucose uptake with or without an infusion of angiotensin II (approximately 15 ng.kg-1.min-1), which increased blood pressure by 20/15 mmHg (systolic/diastolic). Addition of angiotensin II increased whole body glucose uptake by 15% (9.2 +/- 0.5 vs. 10.8 +/- 0.8 mg.kg-1 x min-1; P = 0.011), and glucose oxidation (determined by indirect calorimetry) by 25% (4.0 +/- 0.3 vs. 4.9 +/- 0.4 mg.kg-1 x min-1; P < 0.05) over insulin alone. There was no significant increase in hepatic glucose output during angiotensin II infusion (2.2 +/- 0.1 vs. 2.4 +/- 0.1 mg.kg-1 x min-1; P = NS). We conclude that angiotensin II in pressor doses increases insulin-mediated glucose disposal and oxidation. The mechanism for this may involve a redirection of blood flow into skeletal muscle during angiotensin II infusion or a direct biochemical action of angiotensin II. Although performed in lean normotensive subjects, these results cast doubt on a significant role for angiotensin II in the insulin resistance associated with essential hypertension.

The Effects of Pressor and Sub-Pressor Doses of Angiotensin II on Insulin Sensitivity: A Placebo-Controlled Study

The Effects of Pressor and Sub-Pressor Doses of Angiotensin II on Insulin Sensitivity: A Placebo-Controlled Study

Magnesium pyrrolidone carboxylate infusion reduces angiotensin II pressor response in pregnant women at risk for hypertension

Abstract OBJECTIVE : Our objective was to investigate the possible restoring action of magnesium on vasculars ensitivity to angiotensin 11 in pregnancy. STUDY DESIGN : We studied intraplatelet free calcium and the pressor response to angiotensin II in 10primigravid women (28 to 32 weeks' gestation) at risk for pregnancy induced hypertension on the basis of altered uteroplacental blood velocity waveforms at 20 weeks' gestation, before and after the infusion of 1 gm of magnesium pyrrolidone carboxylate. After the effective pressor dose was achieved or a maximum of 32 ng/kg per minute was reached, we infused 1 gm magnesium pyrrolidone carboxylate and repeated the test. Intraplatelet free calcium was measured by means of fluorescent probes at the beginning and the end of both tests. RESULTS : Six women were classified as refractory to angiotensin II and four as sensitive (effective pressor dose CONCLUSIONS : Magnesium pyrrolidone carboxylate enhances the vascular refractoriness and intracellular free calcium mediates the pressor response to angiotensin II in pregnancy. (Am J Obstet Gynecol 1992;167:885–8.)

Effect of perindopril on cardiovascular hypertrophy of the SHR: Respective roles of reduced blood pressure and reduced angiotensin II levels

The aim was to determine whether cardiovascular hypertrophy in primary hypertension in the spontaneously hypertensive rat (SHR) is induced by increased levels of angiotensin II or by increased blood pressure. SHR were treated from 7 to 15 weeks of age with perindopril to block the in vivo production of A II and concomitantly infused with either a pressor dose of norepinephrine or angiotensin II. At the end of the treatment period, there was no significant difference in the systolic blood pressure in the norepinephrine or angiotensin II-treated groups (201 ± 9 and 208 ± 8 mm Hg, respectively). However, there was a significant increase (p < 0.01) in left ventricle-plus-septum/body weight ratio in angiotensin II compared with norepinephrine-infused SHR (3.72 ± 0.25 and 2.34 ± 0.04 mg/g, respectively) and in aortic medial cross-sectional area (0.55 ± 0.05 and 0.38 ± 0.01 mm 2, respectively). Using an unbiased optical dissector/fractionator technique, the number of smooth muscle cells in the descending thoracic aorta of the angiotensin II-infused SHR was not different from norepinephrine-infused rats (5.02 ± 0.30 × 10 6 and 4.71 ± 0.42 × 10 6 cells, respectively), and no difference in size of enzyme-isolated cells was observed (mode: 1,326 ± 127 μm 3 compared with 1,186 ± 82 μm 3). The results indicate that angiotensin II directly stimulates cardiac and aortic hypertrophy through a mechanism unrelated to its effect on blood pressure. The aortic hypertrophy is not due to an increase in smooth muscle cell size or number and thus must be related to an increase in the extracellular compartment.

Hypertension Secondary to Early-Stage Kidney Disease: The Pathogenetic Role of Altered Cytosolic Calcium (Ca2+) Homeostasis of Vascular Smooth Muscle Cells

We have examined cardiovascular pressor responsiveness to infused norepinephrine (NE) as related to endogenous plasma NE and plasma renin and to platelet free cytosolic (Ca2+) in 36 patients with early-stage kidney disease and 27 matched normal subjects. The 27 hypertensive patients and the normal subjects did not differ in blood volume, plasma renin, and NE; however, the hypertensive patients had a higher exchangeable body sodium content. Basal plasma NE levels, the relationship between plasma NE measured during NE infusion and the corresponding NE infusion rate, as well as the total plasma clearance for NE did also not differ significantly between the two study groups. In contrast, the threshold or pressor doses of infused NE significantly decreased in the patients with kidney disease. Antihypertensive pharmacotherapy with (Ca2+) channel blockers and/or loop diuretics normalized blood pressure and cardiovascular NE hyperresponsiveness and reduced blood volume, exchangeable body sodium, and platelet free cytosolic (Ca2+). In contrast, experimental digitalisation as a model for in vivo sodium/potassium adenosine triphosphatase inhibition augmented NE responsiveness and raised platelet free cytosolic (Ca2+). Incubation of platelets from normal subjects with plasma ultrafiltrate from hypertensive patients gave evidence for an endogenous factor capable to raise free cytosolic (Ca2+) and to act synergistically with digoxin. Hypertension secondary to early-stage kidney disease is related to an impairment of sodium excretion leading to an expansion of blood volume and exchangeable body sodium. This may result in increased secretion of endogenous factors, leading to alterations of cytosolic (Ca2+) homeostasis of vascular smooth muscle cells followed by elevated peripheral resistance and thus blood pressure.

Newer aspects of the reversible inhibitor of MAO-A and serotonin reuptake, brofaromine

Waldmeier, Peter C.: Newer Aspects of the Reversible Inhibitor of MAO-A and Serotonin Reuptake, Brofaromine. Prog. Neuro-Psychopharmacol. & Biol. Psychiat. 1993, 17 :(2) 183–198. 1. 1. The reasons for developing second-generation MAOI are outlined. The expected advantage of reversibility as a safety value with respect to tyramine potentiation is discussed. 2. 2. Earlier data from in vitro and some ex vivo experiments had suggested an irreversible interaction of brofaromine with MAO-A, whereas the short duration of action, the absence of cumulation of effect and the displaceability by endogenously released substrates indicated reversibility. This apparent conflict could be solved by the demonstration that brofaromine behaves as a tight-binding reversible inhibitor. 3. 3. In in vivo binding experiments with [ 3H]brofaromine given i.v., clorgyline, brofaromine and moclobemide were shown to dose-dependently displace the radioligand from MAO-A in the rat brain when administered after it. In corresponding experiments in the rat intestine in which the radioligand was administered p.o., similar results were obtained. Moreover, tyramine given orally in pressor doses after the radioligand also displaced it, confirming the idea that reversibility could act as a safety valve. 4. 4. The evidence from animal and human experiments is presented that brofaromine is safer than classical MAO inhibitors with respect to tyramine potentiation. 5. 5. Based on computer simulations, it is suggested that reduced liability of the new MAO reversible inhibitors to cause tyramine potentiation may potentially be linked to a reduced therapeutic efficacy. 6. 6. The evidence is discussed that 5-HT uptake inhibition by brofaromine is relevant in its therapeutic effect in humans and may synergize with MAO-A inhibition, thus enhancing the impact of the latter on serotonergic transmission.

Dose-related cardiovascular effects of spironolactone

The aim of this study was to assess the shortterm hemodynamic effects of increasing doses of spironolactone (25, 50, and 75 mg/day) on oligurie patients (5 men, mean age 47 ± 12 years) undergoing hemodialysis for chronic renal impairment. Parameters of interest included heart rate (HR), cardiac output, systemic vascular resistance (SVR), arterial pressure, right atrial pressure, and pulmonary capillary wedge pressure (PCWP). The study also evaluated how spironolactone modified the effects on arterial and right atrial pressures and PCWP of infusion of increasing doses of norepinephrine (20, 40, and 100 ng/ kg/min) and angiotensin II (2, 4, and 10 ng/kg/ min). Compared with placebo, the lowest dose of spironolactone (25 mg/day) produced statistically significant (p < 0.05) modifications in systemic arterial pressures without a compensatory increase in cardiac output. The modifications were more pronounced at 50 and 75 mg/day, and the latter had a significant dose-dependent effect. Moreover, doses of 50 and 75 mg/day produced significant (p < 0.05) decreases in right atrial pressure and PCWP. Spironolactone administration caused the curve expressing the relation between an infused norepinephrine or angiotensin II dose and the blood pressure response to shift significantly (p < 0.05 to <0.01) to the right, and the pressor doses of norepinephrine or angiotensin II showed a significant (p < 0.05 to <0.01) dose-related increase, suggesting that treatment with spironolactone inhibited cardiovascular reactivity. This effect was observed on both the capacitance (i.e., low-pressure) and resistance (i.e., high pressure) vessels. Thus, an important dose-related effect of spironolactone on both the high- and low-pressure systems appears to play a major role in the drug's vascular and antihypertensive effects.

Angiotensin II Infusion Affects Fluorescence Polarization and Cholesterol Content of Platelet Membranes

Objective: We studied the modifications of the physicochemical properties and the lipid composition of platelet plasma membranes during angiotensin infusion.Methods: Platelets were obtained during angiotensin II infusion from 8 primigravid women at 25 to 32 weeks' gestation. Fluorescence polarization and cholesterol concentration were measured at the beginning of the test and when the effective pressor dose (EPD, i.e., infusion rate at which diastolic blood pressure rises 20 mm Hg from baseline) was achieved.Main Outcome Measures: The modification of cholesterol/phospholipid ratio and the subsequent modification of polarization of platelet membrane in response to increasing angiotensin II infusion rates were considered.Results: Both fluorescence polarization and cholesterol concentrations of platelet membrane were significantly reduced (ANOVA for repeated measures P <. 001) at the EPD (polarization 0.275 ± 0.004 vs. 0.250 ± 0.003; cholesterol 110.0 ± 4.0 vs. 65.0 ± 5.2 nmol/L, respectively). The infusion ...

The blood pressure response to infusions of angiotensin II during normal pregnancy: Relation to plasma angiotensin II concentration, serum progesterone level and mean platelet volume

Objective: This study is a survey of the determinants of refractoriness to the pressor effects of angiotensin II during normal pregnancy. Study Design: In 25 normal pregnant women, the effective angiotensin II pressor dose was determined 88 times from the twenty-fifth to the thirty-second week of gestation. Immediately before the angiotensin II infusion, blood samples were collected and measured for plasma angiotensin II concentration, serum progesterone level, platelet count, and mean platelet volume. Results: The effective pressor dose had a significantly positive correlation with plasma angiotensin II concentration and serum progesterone level and a negative correlation with mean platelet volume. Conclusion: The pregnancy-associated refractoriness to angiotensin II is physiologically determined, at least in part, by the elevated circulating levels of endogenously produced angiotensin II and by the progesterone produced by the placenta, whereas platelet activation attenuates the relative refractoriness during normal pregnancy.

Intravenous angiotensin II induces Fos-immunoreactivity in circumventricular organs of the lamina terminalis

Conscious rats were infused intravenously with either angiotensin II (30–55 pmol/kg/min), isotonic saline or phenylephrine for 2 h, then killed. Fos was identified by immunohistochemistry in the brains. Fos expression occurred in many neurons of the subfornical organ and organum vasculosum of the lamina terminalis (OVLT) with angiotensin infusion but not with isotonic NaCl or phenylephrine. Fos immunoreactivity was induced in cells in several medullary, hypothalamic and limbic structures with infusions of angiotensin II or phenylephrine at pressor doses. The results suggest that blood-borne angiotensin II at physiological levels causes angiotensin receptive neurons in the subfornical organ and OVLT to express Fos. Activation of baroreceptor pathways may also induce Fos expression at several other sites.

Magnesium pyrrolidone carboxylate infusion reduces angiotensin II pressor response in pregnant women at risk for hypertension

OBJECTIVE: Our objective was to investigate the possible restoring action of magnesium on vasculars ensitivity to angiotensin 11 in pregnancy. STUDY DESIGN: We studied intraplatelet free calcium and the pressor response to angiotensin II in 10primigravid women (28 to 32 weeks' gestation) at risk for pregnancy induced hypertension on the basis of altered uteroplacental blood velocity waveforms at 20 weeks' gestation, before and after the infusion of 1 gm of magnesium pyrrolidone carboxylate. After the effective pressor dose was achieved or a maximum of 32 ng/kg per minute was reached, we infused 1 gm magnesium pyrrolidone carboxylate and repeated the test. Intraplatelet free calcium was measured by means of fluorescent probes at the beginning and the end of both tests. RESULTS: Six women were classified as refractory to angiotensin II and four as sensitive (effective pressor dose <10 ng/kg per minute). After magnesium pyrrolidone carboxylate infusion, the four sensitive women became refractory and the effective pressor dose was significantly enhanced to 32 in all six refractory women. Intracellular free calcium increased significantly during the first angiotensin II infusion, whereas after magnesium pyrrolidone carboxylate administration it did not change significantly. CONCLUSIONS: Magnesium pyrrolidone carboxylate enhances the vascular refractoriness and intracellular free calcium mediates the pressor response to angiotensin II in pregnancy. ( Am J Obstet Gynecol 1992;167:885–8.)

Effects of endothelin on renal hemodynamics and tubuloglomerular feedback.

The effect of endothelin (ET)-1 infusion on renal hemodynamics and the tubuloglomerular feedback (TGF) mechanism was examined in rats. ET-1 reduced early proximal flow rate (EPFR) measured in the absence of distal flow from 28 +/- 1 to 23 +/- 1 nl/min at a subpressor dose (100 pmol.100 g body wt-1.h-1 iv) and from 27 +/- 2 to 19 +/- 2 nl/min at a pressor dose (200 pmol.100 g body wt-1.h-1). Reductions of EPFR induced by loop perfusion at 40 nl/min were 11 +/- 1 and 12 +/- 1 nl/min at the subpressor and pressor doses and were not different from controls. The stop-flow pressure response to loop perfusion was not altered by the pressor dose of ET-1. The subpressor dose of ET-1 increased renal vascular resistance (RVR) by 40% but left glomerular filtration rate (GFR) and urinary excretion of sodium (UNaV) unaltered. The pressor dose of ET-1 not only increased RVR by 140% and decreased GFR and renal plasma flow by 37 and 52%, but it increased UNaV proportional to the rise in blood pressure (r = 0.724, P less than 0.01). ET-1 is a potent renal vasoconstrictor and induces pressure natriuresis. ET-1 increases both pre- and postglomerular resistances but does not affect TGF response.

Baroreflex modulation of sympathetic outflow during physiological increases of vasopressin in humans.

Two studies were carried out to determine whether vasopressin influences the baroreceptor reflex of humans. In protocol 1, eight healthy subjects received sequential infusions of nitroprusside and phenylephrine to alter baroreceptor input. Muscle sympathetic nerve activity (SNA) was recorded to assess baroreceptor reflex modulation of efferent vasoconstrictor drive. Baroreceptor sensitivity (slopes) of the relationship between systolic pressure and R-R interval (cardiac baroslopes) and slopes relating muscle SNA to diastolic pressure were not altered during subpressor infusions of vasopressin, which raised basal plasma levels to 19 +/- 6 and 26 +/- 6 (mean +/- SE) pg/ml. A second protocol (n = 10 subjects) compared the reflex inhibition of SNA and heart rate produced by incremental pressor doses of phenylephrine and vasopressin. The calculated cardiac and sympathetic baroreflex gains did not differ between pressor agents. However, immediately following the peak dose of vasopressin (which elevated plasma levels to 35 +/- 3.6 pg/ml), reflex sympathoexcitation produced by unloading baroreceptors (with a bolus of nitroprusside) was significantly enhanced compared with an identical stress initiated at peak phenylephrine infusion. Thus increased levels of vasopressin ranging from 19 to 26 pg/ml did not alter cardiac or sympathetic baroreflex responses in humans. Higher levels of vasopressin may enhance the sympathetic response to unloading of baroreceptors.

The blood pressure response to infusions of angiotensin II during normal pregnancy: Relation to plasma angiotensin II concentration, serum progesterone level, and mean platelet volume

This study is a survey of the determinants of refractoriness to the pressor effects of angiotensin II during normal pregnancy. In 25 normal pregnant women, the effective angiotensin II pressor dose was determined 88 times from the twenty-fifth to the thirty-second week of gestation. Immediately before the angiotensin II infusion, blood samples were collected and measured for plasma angiotensin II concentration, serum progesterone level, platelet count, and mean platelet volume. The effective pressor dose had a significantly positive correlation with plasma angiotensin II concentration and serum progesterone level and a negative correlation with mean platelet volume. The pregnancy-associated refractoriness to angiotensin II is physiologically determined, at least in part, by the elevated circulating levels of endogenously produced angiotensin II and by the progesterone produced by the placenta, whereas platelet activation attenuates the relative refractoriness during normal pregnancy.

Low-Dose Aspirin Qualitatively Affects the Vascular Response to Angiotensin II in Hypersensitive Pregnant Women

Forty-four women underwent an angiotensin sensitivity test (AST) at 32.4±35 (mean±SD) weeks of gestation. They were divided into two groups according to the effective pressor dose (EPD) and were defined as AST positive (n=17) or AST negative (n=27) if the EPD was <10 or ±10 nanograms/Kg/min, respectively. A regression line of the diastolic blood pressor response to angiotensin II (A II) was obtained for each woman and the mean dose:response curve for each of the two groups was computed. The mean dose:response curves from the AST positive and AST negative groups show no difference between the intercepts (−91±8.2 vs −7.3±6.6, respectively; p NS), but significant difference between the slopes (34.3±8.9 vs 195±72; p<0.00001) and the calculated thresholds (2.6±1.0 vs 4.8±2.4; p<0.001). The administration of 100 mg per day aspirin for 7 days significantly lowered the slope of the mean dose:response curve in the AST positive group with no effect on that of the AST negative group, so resulting in two very similar...