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Biomedical subjects

A Morganti

Publications and source records attributed to A Morganti.

At least 37 records · Page 2Linked to original sources
PubMed1996

Superiority of acceleration and acceleration time over pulsatility and resistance indices as screening tests for renal artery stenosis.

OBJECTIVE: To compare the accuracy of four echo-Doppler-derived velocimetric indices (pulsatility and resistance indices, acceleration and acceleration time) in detecting renal artery stenosis in hypertensive patients. PATIENTS AND METHODS: In 73 hospitalized patients with moderate-to-severe hypertension, 18 of whom had normal renal arteries and 55 renal artery stenosis (50-95%) either atherosclerotic (30 cases, five bilateral) or fibromuscular dysplasia (25 cases, two bilateral), we measured the four velocimetric indices using the lateral abdominal approach and sampling Doppler waveforms distally to the stenosis. The diagnostic accuracy of each index was calculated using as cut-off limit the ideal threshold determined with the receiver-operating characteristic curves. RESULTS: On average all of the indices were altered significantly in arteries with stenosis of both aetiologies with respect to normal arteries, the alterations of pulsatility and resistance indices being, however, less pronounced than those of acceleration and acceleration time, particularly in atherosclerotic stenosis. With the cut-off limits of 0.93, 0.59 and 7.4 m/s2 and 60 ms, respectively, for pulsatility and resistance indices, acceleration and acceleration time, their diagnostic accuracies were 80, 73, 93 and 92%. In stenotic arteries, only the acceleration time was correlated with the degree of arterial narrowing, whereas, in normal arteries, only pulsatility and resistance indices were directly correlated with the age of patients. CONCLUSIONS: Acceleration and acceleration time are more accurate indices than pulsatility and resistance to screen for renal artery stenosis, probably because their alterations are less attenuated by the counterbalancing effects of age and of atherosclerosis.

Acceleration↗
PubMed1996

Humoral effects of selective adenosine agonists in spontaneously hypertensive rats.

OBJECTIVE: We studied the dose-response effects of acute administration of the selective A1 adenosine receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA), the selective A2A agonists 2-hexynyl-5'-N-ethylcarboxamidoadenosine (2HE-NECA) and 2-[4-(2-carboxyethyl)phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS 21680) and the non-selective agonist N-ethylcarboxamidoadenosine (NECA) on plasma renin activity, atrial natriuretic peptide, cyclic guanosine 3',5'-monophosphate (cGMP) and endothelin-1 in spontaneously hypertensive rats. METHODS: The drugs were administered intraperitoneally in four doses to conscious rats. Systolic blood pressure and heart rate were measured by the tail-cuff technique. Both humoral and hemodynamic parameters were determined 1 h after dosing in separate sets of animals. RESULTS: All the compounds induced a dose-dependent decrease in systolic blood pressure that was associated with different changes in heart rate. Heart rate was decreased by all doses of CCPA and by the higher doses of the non-selective compound (NECA) and increased by both A2A agonists. Plasma renin activity also changed in opposite directions, being decreased by CCPA but increased dose-dependently by 2HE-NECA and CGS 21680 and only moderately by NECA. Plasma atrial natriuretic peptide and cGMP levels increased dose-dependently after CCPA and NECA, but were unaffected by the A2A agonists. None of the compounds altered plasma endothelin-1 levels. CONCLUSIONS: These results indicate that the renin-suppressive effect of the A1 agonist, which is associated with a cardiodepressant action, may be attributed either to a direct inhibition of renin release or to the concomitant increments in plasma atrial natriuretic peptide and its second messenger, cGMP. In contrast, the renin-stimulating effect of the A2A agonists may result either from direct stimulation of renin secretion or from reflex sympathetic activation secondary to the fall in blood pressure.

Adenosine↗
PubMed1995

Effects of exposure to high altitude on plasma endothelin-1 levels in normal subjects.

OBJECTIVE: To assess whether the hypoxia associated with exposure to high altitude affects plasma endothelin-1 levels, and whether changes in endothelin-1 are related to those in systemic and pulmonary blood pressure. DESIGN: Eight normal subjects ascended Mount Everest to an altitude of 5050 m within a period of 8 days (study 1) and 10 ascended Mount Rosa in the Italian Alps to an altitude of 4559 m within 2 days (study 2). In study 1 systemic blood pressure, heart rate, haematocrit, haemoglobin oxygen saturation (evaluated by percutaneous oximetry) and venous plasma endothelin-1 were measured several times during the ascent, and twice more during the time spent at high altitude. In study 2 the same parameters as well as systolic pulmonary pressure by echocardiography were evaluated on the second day of resting at 4559 m. In both studies, data obtained during the expeditions were compared with those collected from the same subjects at sea level. RESULTS: In study 1 plasma endothelin-1 increased progressively up to 4240 m (from 1.8 +/- 0.1 pg/ml at sea level to 2.7 +/- 0.2 pg/ml) and decreased slightly thereafter; these increments were directly related to the decrements in percutaneous oxygen saturation, which, at that altitude, fell from 98.6 +/- 0.2% at sea level to 80.8 +/- 0.4%. Blood pressure and haematocrit also rose in response to exposure to high altitude but these changes were not related to changes in endothelin-1. In study 2 the increments in plasma endothelin-1 were similar to those observed in study 1 and the changes again correlated with changes in oxygen saturation as well as with those in systolic pulmonary pressure. On average, systolic pulmonary pressure increased from 19 +/- 1 to 26 +/- 1.9 mmHg, whereas systemic blood pressure and haematocrit were unchanged. CONCLUSION: Exposure to high altitude is associated with consistent increases in plasma endothelin-1. This is probably the result of augmented secretion of the peptide in response to hypoxia and may contribute to the physiological adaptation of the pulmonary circulation to this condition.

Adult↗
PubMed1995

Atrial natriuretic peptide and hemodynamic changes during normal human pregnancy.

We compared plasma atrial natriuretic peptide (ANP) and cGMP levels during normal pregnancy--a condition characterized by hypervolemia, high cardiac output, and decreased vascular resistance--with postpartum levels and assessed their relation to pregnancy-induced hemodynamic changes. Humoral and hemodynamic variables were measured in healthy women subjects in the supine and upright postures at each trimester of pregnancy and postpartum. Supine plasma ANP was increased throughout pregnancy (32 +/- 5, 21 +/- 3, and 19 +/- 2 versus 15 +/- 1 pmol.L-1, respectively, at each trimester versus postpartum), as was cGMP (8.6 +/- 1, 7.1 +/- 1, and 6.6 +/- 1 versus 5.6 +/- 1 nmol.L-1), and their increments were directly related (r = .68, P < .01). Both ANP and cGMP levels did not differ from postpartum levels after subjects stood. Supine stroke volume was initially increased but declined below postpartum levels in late pregnancy (69 +/- 4, 60 +/- 3, and 44 +/- 3 versus 58 +/- 4 mL.m-2), whereas after subjects stood it was always higher (56 +/- 3, 58 +/- 3, and 49 +/- 2 versus 44 +/- 2 mL.m-2); thus, stroke volume tended to increase in response to standing in late pregnancy. Supine cardiac index had a similar trend, which was opposite to that of total peripheral resistance (1213 +/- 62, 1265 +/- 79, and 1729 +/- 89 versus 1654 +/- 92 dyne.s-1.cm-5.m-2).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Immunoradiometric versus enzymatic renin assay: results of the Italian Multicenter Comparative Study. Italian Multicenter Study for Standardization of Renin Measurement.

OBJECTIVES: The measurement of plasma renin activity (PRA) is very convenient for estimating the action of the renin system, but its interlaboratory reproducibility is notoriously poor. This multicentre study aimed to examine whether an immunoradiometric assay which quantifies renin directly with monoclonal antibodies can reduce this limitation of the enzymatic assay. The study also aimed to establish the reference values of immunoreactive renin (IrR) in a large sample of normotensive subjects and patients with various pathophysiological conditions. DESIGN AND METHODS: PRA and IrR were measured once in each of the eight participant centres in eight pool plasma samples with a wide range of renin content; in seven centres these measurements were repeated twice more in order to compare the intralaboratory interassay reproducibility of both methods. Finally, PRA and IrR were measured in the supine and standing positions in 503 subjects including normal controls, patients with various forms of hypertension, patients with Cushing's and Bartter's syndromes, patients with hepatic cirrhosis and pregnant women. RESULTS: We found that both the inter- and intralaboratory coefficients of variation for PRA measurements were higher than those for IrR. In plasma samples from normal subjects and from patients, mean +/- SEM supine PRA and IrR ranged, respectively, from 0.08 +/- 0.03 ng/ml per h and 2.6 +/- 0.5 pg/ml in patients with Conn's syndrome to 7.2 +/- 2.5 ng/ml per h and 138 +/- 51 pg/ml in patients with hepatic cirrhosis. PRA and IrR were found to be significantly correlated in all laboratories (mean +/- SEM of correlation coefficients 0.84 +/- 0.03) and for all of the conditions (correlation coefficient ranging from 0.98 in patients with Cushing's syndrome to 0.50 in pregnant women). However, for the pregnant women the slope of the regression line depicting the PRA-IrR relationship was significantly steeper than for all of the other conditions. CONCLUSIONS: In our experience the inter- and intralaboratory reproducibilities of the immunoradiometric assay appear to be greater than can be achieved with the enzymatic assay, the difference being probably due to the greater complexity of the latter. The two methods provide superimposable information on the renin-angiotensin system activity, except in pregnancy, during which the PRA:IrR ratio is much higher than in the other conditions. Therefore, in this and other pathophysiological situations associated with marked angiotensinogen concentration alterations, the enzymatic assay may be still preferable for assessing the activity of the system accurately.

Adolescent↗
PubMed1994

Hemodynamic and humoral effects of chronic treatment with the neutral endopeptidase inhibitor SCH 42495 in spontaneously hypertensive rats.

Blockade of atrial natriuretic factor (ANF) degradation by specific neutral endopeptidase (NEP) inhibitors may be useful in treatment of hypertension because of the potential diuretic, natriuretic, and arterial pressure (AP)-lowering effects. To test this possibility, we examined the effects of chronic oral treatment with the NEP inhibitor SCH 42495 on BP, diuresis, natriuresis, plasma ANF, cyclic GMP, and the renin-angiotensin system (RAS) in conscious unrestrained spontaneously hypertensive rats (SHR) and compared them with the effects induced by the angiotensin-converting enzyme (ACE) inhibitor spirapril (SPIR). Four groups of adult SHR were treated orally for 4 weeks with placebo, SCH 42495 3 mg/kg twice daily (b.i.d.), SCH 42495 30 mg/kg b.i.d., and spirapril 1 mg/kg b.i.d. Systolic BP (SBP) was measured weekly, and 24-h urine was collected every week for measurement of urinary volume, sodium, potassium, and cyclic GMP excretion. Plasma ANF, cyclic GMP, renin activity (PRA), and aldosterone (ALDO) were determined from blood collected when the rats were killed. After 4-week treatment with SCH 42495, circulating levels of ANF were similar in both SCH 42495- and placebo-treated SHR; plasma cyclic GMP was higher, however, in the treated rats than in controls and urinary cyclic GMP increased only with the higher dose of SCH 42495. PRA and plasma ALDO tended to be lower in both SCH 42495-treated groups than in controls, yet BP, diuresis, and natriuresis throughout the study were not different from controls. In contrast, spirapril decreased BP; this effect was associated with significant increments in renin and decrements in ALDO and ANF, without changes in plasma and urinary cyclic GMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1994

Effect of atrial natriuretic factor infusion on basal and CRH-stimulated ACTH, cortisol and aldosterone levels in patients with Cushing's or Addison's disease.

OBJECTIVE: While it has been shown that atrial natriuretic factor (ANF) is able to inhibit CRH-stimulated ACTH secretion in vitro, in normal men conflicting results on its effect on ACTH/cortisol responses to insulin and CRH have been reported. Since no data are available concerning the possible influence of ANF on the hypothalamic-pituitary-adrenal axis in states of ACTH hypersecretion, the effect of ANF on pituitary-adrenal function in basal conditions and after CRH stimulation has been investigated in patients with Cushing's (n = 4) and Addison's disease (n = 4). DESIGN: On two different days all patients underwent the following procedures: (a) alpha-human ANF was infused, after a priming dose of 100 ng i.v., at a rate of 0.01 microgram/kg/min over 5 hours. After 120 minutes of ANF infusion, oCRH (1 microgram/kg) was i.v. injected as a bolus; (b) vehicle infusion was given over 5 hours and at 120 minutes oCRH was injected. Plasma ANF, ACTH, cortisol, aldosterone, renin activity and K+ were measured; heart rate and blood pressure were monitored. RESULTS: In Cushing's disease plasma ANF rapidly increased within 30 minutes of the exogenous peptide infusion (from 27 +/- 5 to 73 +/- 14 pmol/l; mean +/- SE), whereas in the vehicle study its concentration was unchanged. During the first 2 hours of both tests no significant modifications in ACTH levels were observed. After CRH the plasma ACTH peak was unchanged. Serum cortisol levels progressively declined during the first 2 hours of ANF infusion (from 778 +/- 150 to 461 +/- 48 nmol/l; P < 0.05), whereas no changes were observed during vehicle. After CRH serum cortisol rose to similar peaks. Plasma aldosterone levels were significantly reduced during the first 2 hours of ANF infusion (from 81 +/- 20 to 35 +/- 7 pmol/l P < 0.05), whereas no changes were found during vehicle. A similar aldosterone rise was induced by CRH during either vehicle or ANF. Mean plasma renin activity slightly declined and the changes were similar on both occasions. In Addison's disease ANF levels rose within 30 minutes of the peptide infusion (from 12 +/- 1 to 49 +/- 8 pmol/l), while they were unchanged during vehicle. A slight decline in ACTH levels in the first 2 hours was observed during either vehicle or ANF infusion. After CRH the plasma ACTH peaks were similar. Mean plasma renin activity was unaffected by vehicle, while ANF caused a decline during the first 2 hours (from 13.4 +/- 0.8 to 7.7 +/- 0.3 ng/ml/h). In all patients, heart rate, blood pressure and K+ were only slightly affected on both occasions. CONCLUSIONS: (1) In patients with corticotrophin hypersecretion ANF does not influence basal and CRH-stimulated ACTH secretion; (2) in Cushing's disease ANF inhibits cortisol and aldosterone basal secretion; this effect is not mediated by ACTH and is over-ridden by CRH stimulation.

Addison Disease↗
PubMed1994

Validation study of thoracic fluid bioimpedance for assessing the haemodialysis-induced changes in total body fluids.

Thoracic fluid bioimpedance (TFB) has been proposed as a noninvasive technique for monitoring both haemodynamics and fluid homeostasis in patients on regular dialysis. To validate the reliability of TFB in assessing the haemodialysis (HD)-induced changes in plasma volume (PV) in these patients, we examined the changes of TFB during and after HD in relation to those in total plasma protein (TP) concentration, haematocrit (Ht), heart rate (HR), total body water (TBW) and plasma angiotensin II (A-II) concentration. Data were recorded in 13 HD patients with a wide range of interdialytic weight gains before, at the end, and 4, 8, 24, 48 h after the HD session. We found that the percent TFB changes were closely and inversely related with those of TP, Ht and TBW (r = -0.54, r = -0.45 and -0.68, respectively, p < 0.001 for all). Similar relations were found between the percent changes in TFB and those in absolute TP and Ht. In addition, a direct relation was found between the percent changes of TFB and those of HR and of A-II (r = 0.33 and r = 0.31, respectively, p < 0.01 for both). These data indicate that TFB is a reliable method for evaluating the HD-induced changes of intra- and extravascular fluids and, with respect to the conventional techniques, has the advantage of providing this information dynamically, and in conjunction with the haemodynamic data of patients.

Adult↗
PubMed1994

Endothelin-releasing stimuli and calcium antagonists in normal and pathological conditions.

BACKGROUND: Endothelin-1 is a potent vasoconstrictive peptide which circulates in blood at very low concentrations. It is mostly released from endothelial cells towards the vascular smooth muscle cells. Therefore studies addressed at increasing endothelin-1 production using physical stimuli may easily fail to cause sizeable modifications in plasma endothelin levels. Upright posture and exposure to cold, the two maneuvers so far most commonly used in humans, often have inconsistent effects on plasma endothelin-1. RECENT FINDINGS: In recent studies we have found that exposure to high altitude (4500-5000 m) caused, in normal subjects, significant increases in endothelin-1 which were correlated with those of mean arterial pressure and of systolic pulmonary pressure. CONCLUSIONS: Hypobaric hypoxia appears to stimulate the secretion of endothelin-1 and this response may contribute to the adaptation by the systemic and pulmonary circulation to the stress of altitude. If this can be confirmed, calcium antagonists, which are known to antagonize endothelin-1 mediated vasoconstriction, may be used to alleviate the pulmonary hypertension that occasionally occurs under these specific circumstances.

Calcium Channel Blockers↗
PubMed1993

Coronary blood flow in renovascular hypertension.

We assessed the acute effects of 2.5 mg oral cilazapril on systemic and coronary hemodynamics in seven renovascular hypertensive patients with a chronically overactive renin-angiotensin system (RAS), but with no electrocardiographic or echocardiographic signs of left ventricular hypertrophy. Cilazapril resulted in a significant decrease in mean arterial pressure and coronary vascular resistance, together with a prolonged increase in coronary sinus blood flow (CSBF). Post-cilazapril handgrip resulted in larger increases in CSBF in response to a given increase in myocardial oxygen requirements. It is concluded that the chronic activation of the RAS exerts an adverse influence on the control mechanisms of CSBF and that converting enzyme inhibition reverses the effects of angiotensin II on coronary hemodynamics. Converting enzyme inhibitors may have a cardioprotective role in renovascular hypertension.

Adult↗
PubMed1993

Abnormal hemodynamics and elevated angiotensin II plasma levels in polydipsic patients on regular hemodialysis treatment.

To investigate the cause and the mechanisms responsible of the compulsive thirst and excessive fluid intake observed in many patients on chronic dialysis treatment, we measured plasma antidiuretic hormone (ADH), angiotensin II (Ang II) and some hemodynamic parameters in seven polydipsic and in six normodipsic patients before hemodialysis, at the end of it and several times during the interdialytic interval. Before dialysis we found that ADH was elevated in both groups (6.9 +/- 1.9 vs. 6.9 +/- 1.3 pg/ml, respectively in polydipsics and controls), whereas Ang II was abnormally high only in polydipsics (51 +/- 12 vs. 11 +/- 3 pg/ml, P < 0.01); these patients also had significantly higher heart rate and cardiac indices and lower total peripheral resistances than control patients. Overall these hemodynamic indices were related with Ang II but not with ADH. Ang II rose markedly in polydipsics after dialysis, reaching a peak at the fourth hour after its termination (136 +/- 12 pg/ml) and remained consistently elevated throughout the interdialytic period, whereas in controls Ang II was practically unchanged with respect to baseline. In contrast, ADH had minor and similar modifications in both groups, in whom also the hemodynamic changes were superimposable. Significant correlations were found between the absolute and percent changes of Ang II and those of plasma volume during the interdialytic interval (P < 0.001 for both), and between the individual values of Ang II measured during the whole study and the interdialytic weight gain (P < 0.05). These results demonstrate that polydipsic patients have abnormally high levels of Ang II before and after the hemodialysis-induced volume depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Whole liver intraoperative irradiation after partial hepatectomy produces minimal functional and pathologic lesions.

Intraoperative radiation therapy (IORT) was delivered to remnant rat liver after partial hepatectomy to determine the chronic effects of treatment on survival, blood chemistry, liver weight, and histology. Survival at one year was 100%. Remnant liver weight was markedly increased in all animals. Liver function appeared to be unaltered in all groups and at all observation times. Inflammatory cell infiltration occurred immediately after treatment in all animals, showing a slight progression until day 45; by day 180 the values had returned to baseline. Vascular changes were seen early in all groups, then progressively decreased; the vascular score was back to baseline at days 180 and 365. Nuclear alterations were observed in both irradiated and nonirradiated hepatic cells; in all cases these were limited to isolated or focal areas of hepatocytes. There was little fibrosis formation and by day 180 all scores were back to baseline. We conclude that the chronic effects of whole liver IORT after one-third hepatectomy are minimal in the rat and are similar to those observed after surgery alone.

Animals↗
PubMed1992

Sympathomoderating influence of benazepril in essential hypertension.

OBJECTIVE: In essential hypertension, captopril attenuates forearm vasoconstriction reflexly induced by deactivation of cardiopulmonary and arterial baroreceptors, thus exerting a sympathomoderating effect. We investigated whether this is a common effect of angiotensin converting enzyme (ACE) inhibitors. METHODS AND DESIGN: Cardiopulmonary and arterial baroreceptors were deactivated by progressively reducing central venous pressure (CVP) through progressively greater lower body negative pressures in eight untreated mild essential hypertensives on a moderately low-sodium diet (50 mmol/l per day). This deactivation was performed after oral administration of the non-sulphidrylic ACE inhibitor benazepril (10 mg) and placebo according to a double-blind randomized crossover experimental design. RESULTS: After placebo, the reduction in CVP increased forearm vascular resistance (FVR; mean arterial pressure: plethysmographic forearm blood flow ratio). After benazepril, baseline blood pressure (beat-to-beat finger pressure) and FVR were significantly reduced whilst plasma angiotensin II was suppressed and PRA increased (both measured by radioimmunoassay). The FVR increases induced by progressive CVP reduction were less than after placebo administration, and the overall difference was statistically significant. Benazepril did not affect the reflex FVR reduction observed by increasing CVP through leg raising, nor the reflex changes in plasma norepinephrine measured by high-performance liquid chromatography accompanying the changes in FVR. CONCLUSIONS: Benazepril attenuates sympathetic vasoconstriction as does captopril. This effect (which is mainly operative during an increased sympathetic drive and exerted through a reduction of adrenoceptor responsiveness) is thus likely to be a class- rather than a compound-related feature.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

ACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease.

BACKGROUND: In humans, angiotensin converting enzyme (ACE) inhibition attenuates the vasoconstriction induced by sympathetic stimulation in a number of peripheral districts. Whether this is also the case in the coronary circulation is unknown, however. METHODS AND RESULTS: In nine normotensive patients with angiographically assessed coronary atherosclerosis, we measured the changes in mean arterial pressure (intra-arterial catheter), heart rate, rate-pressure product (RPP), coronary sinus blood flow (CBF, thermodilution method), and coronary vascular resistance (CVR, ratio between mean arterial pressure and CBF) induced by the cold pressor test (CPT, 2 minutes) and diving (30 seconds), i.e., two stimuli eliciting a sympathetic coronary vasoconstriction. The measurements were performed in the control condition and 30 minutes after captopril 25 mg p.o. In the control condition, CPT caused an increase in mean arterial pressure and heart rate. Despite the increase in RPP (+20.7 +/- 3.2%, p less than 0.01), CBF did not change and CVR increased (+12.2 +/- 4.0%, p less than 0.05). diving caused an increase in mean arterial pressure and a reduction in heart rate. RPP increased (+14.3 +/- 3.5%, p less than 0.01), but despite this increase, there was a reduction in CBF and a marked increase in CVR (+37.3 +/- 7.4%, p less than 0.01). Captopril did not modify the blood pressure and heart rate responses to both stimuli except for a slight accentuation of the bradycardia to diving. Despite the unchanged or only slightly reduced RPP response, the increase in CVR was markedly and significantly attenuated (p less than 0.01). CONCLUSIONS: ACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease. This is probably due to removal of the facilitating influence of angiotensin II on sympathetic modulation of coronary vasomotor tone.

Angiotensin II↗
PubMed1992

Acute effects of cilazapril on coronary hemodynamics in patients with renovascular hypertension.

The effects of converting enzyme inhibition on coronary and systemic hemodynamics in the presence of a chronically activated renin-angiotensin system were investigated in five renovascular hypertensive patients with no ECG/echocardiographic evidence of left ventricular hypertrophy. Coronary blood flow (CBF, thermodilution technique), intra-arterial blood pressure, AVO2 difference (coronary sinus), heart rate, and coronary vascular resistance were measured at rest, during isometric exercise (handgrip to 50% of maximal effort for 3 min) before and 60 min after 2.5 mg of oral cilazapril. The drug induced a prompt, significant decrease in mean arterial pressure and a sustained increase in CBF. The performance of handgrip after cilazapril resulted in higher increases in CBF for a given increase in myocardial oxygen requirements. These observations suggest that angiotensin II (Ang II) maintains the ability to alter the control mechanisms of CBF even under long-term conditions and that converting enzyme inhibition reverses the Ang II-induced effects on coronary hemodynamics.

Adult↗
PubMed1991

Regulation of vasopressin release in moderately severe essential hypertension.

Vasopressin plasma concentrations have been measured in two groups of subjects, 13 moderate essential hypertensive patients without target organ damage and eight control normotensive subjects, before and after the assumption of the upright position, and intravenous infusions of hypotonic saline (0.45% NaCl, 0.25 ml kg-1 min-1 for 1 h) and hypertonic saline (100 mmol NaCl in 50 ml). Plasma vasopressin in recumbent baseline conditions was not significantly different in the two groups. Upright posture and hypertonic challenge augmented, while hypotonic saline reduced plasma vasopressin levels, which were not significantly different between the two groups. Plasma renin activity increased in the upright position, was reduced by administration of hypotonic saline and unaffected by hypertonic saline, with no differences between the hypertensives and normotensives. After hypertonic saline, urinary flow rate and urinary sodium excretion in the hypertensive group increased to values significantly (p less than 0.05) higher than in normotensive subjects. In conclusion our study excludes significant alteration of vasopressin regulation in moderate uncomplicated hypertension. In hypertensives although the response of vasopressin to an osmotic load is preserved, the data suggest that the renal handling of the osmotic load may be altered.

Adult↗