Decrease In Peripheral Vascular Resistance Research Articles

Comparison of blood pressure response to heat stress in sauna in young hypertensive patients treated with atenolol and diltiazem

A sauna bath induces a marked increase in heart rate and a decrease in peripheral vascular resistance as a consequence of heat-induced peripheral vasodilation. 1,2 In normotensive patients the heat stress of a sauna does not change blood pressure (BP). However, a decrease in BP is evident in hypertensive patients, 3 with a risk of hypotensive symptoms after sauna. 1,4 Surprisingly little is known about the impact of cardiovascular drugs on the hemodynamic changes induced by heat stress. Because the β-blocking agent propranolol causes bradycardia, patients are warned of a hypotensive effect after sauna. 4 Calcium antagonists may, by peripheral vasodilation, have an additive effect on the dilation induced by heat stress. 5,6 However, no studies on this topic have been published. In the present study we compared the hemodynamic changes during and after heat stress caused by sauna bath in young hypertensives treated with the calcium antagonist diltiazem and the β 1-selective adrenoceptor antagonist atenolol. We evaluated the possible additive vasodilatory effects of heat stress and calcium antagonists, and the tendency toward hypotensive reactions during and after a sauna bath.

Cardiorespiratory effects of immunotherapy with interleukin-2.

The administration of interleukin 2 (IL-2) and lymphokine-activated killer (LAK) cells can mediate the regression of cancer. Treatment with IL-2 is associated with significant cardiorespiratory effects, as well as a leaky capillary syndrome requiring careful fluid management. A mild reversible depression of cardiac function is also associated with IL-2 treatment. All patients treated with recombinant IL-2 alone, with transfer of LAK cells, or with cyclophosphamide between December 1984 and September 1987 (total of 423 treatment courses in 317 total patients) were evaluated as to the development of significant cardiorespiratory toxicity. Of the 423 treatment courses, only 1.8% were associated with severe peripheral edema and only 2.8% and 3.1% respectively, were associated with significant ascites or pleural effusions. Thirty-nine of 423 patients (9.2%) had severe respiratory distress and 27 patients required intubation (6.4%). Cardiovascular effects included tachycardia and hypotension requiring vasopressor administration in 65% and intravenous (IV) fluid administration. Weight gain greater than or equal to 10% of body weight was noted in 32% of the 423 patients. Arrhythmias were primarily supraventricular (9.7%) and responded well to conventional medical treatments. Angina or ischemic changes were noted in 2.6% of patients and myocardial infarction in 1.2%. IL-2 caused peripheral vasodilation, with a significant decrease in peripheral vascular resistance (2,254 +/- 398 v 1,303 +/- 351 dyne.s.cm-5, P less than .0001), and an increase in heart rate (66.2 +/- 10 v 104.3 +/- 9.6 beats/min, P less than .0001). There was also evidence of mild cardiac dysfunction, with a significant decrease in the left ventricular stroke work (LVSW) index (P less than .0001) and ejection fraction (LVEF) (from 58% +/- 10% to 52% +/- 9%, P less than .03). A repeat LVEF performed after 1 to 3 months, had returned to baseline values (60% +/- 10%). A mean 64% increase in the rate of disappearance of radioactive iodine (125I) albumin (P less than .05) consistent with the development of a leaky capillary syndrome was noted. Patients with underlying cardiorespiratory diseases may be at greater risk during IL-2 administration and should not be selected to undergo this treatment.

Why are converting enzyme inhibitors vasodilators?

1. The primary action of the converting enzyme inhibitors to prevent the formation of angiotensin II can explain a decrease in peripheral vascular resistance in patients with elevated, but not in those with normal or reduced plasma renin levels. 2. The inhibition of the breakdown of bradykinin will potentiate the vasodilator properties of the endogenously produced peptide. These include direct relaxation of certain vascular smooth muscle, production of vasodilator prostanoids and release of endothelium-derived relaxing factor(s). The greater release of the latter in the kidney could exert a negative feedback on the release of renin. 3. In addition, converting enzyme inhibitors may directly (by a prejunctional effect) and indirectly (by curtailing the production of angiotensin II) reduce the release of noradrenaline in the blood vessel wall. 4. Converting enzyme inhibitors may also directly reduce the responsiveness of vascular smooth muscle to vasoconstrictor stimuli (e.g. alpha-adrenoceptor activation). 5. The different effects of these therapeutic agents may concur to induce peripheral vasodilatation.

Serial measurements of cerebral blood flow velocity in preterm infants during the first 72 hours of life.

Serial measurements of cerebral blood flow velocity (CBFV) were made in 29 preterm infants, using continuous wave Doppler ultrasound. CBFV was measured in both anterior cerebral arteries and quantitative measurements of CBFV were determined using the area under the velocity curve. In all ventilated infants, CBFV increased significantly during the first 6 hours of life and continued to increase until 16 hours of age. Thereafter, CBFV remained relatively constant. This increase in CBFV was primarily the result of increased diastolic flow. Three infants who had evidence of intraventricular haemorrhage on cranial ultrasound, had similar CBFV compared with the infants with no evidence of haemorrhage. Two infants died and both demonstrated areas of periventricular leukomalacia at autopsy. These infants had a prolonged period of low CBFV. These measurements provide normal data for ventilated, preterm infants. As previously suggested in term infants, the initial rise in CBFV may be secondary to closure of the ductus although a generalized decrease in peripheral vascular resistance could also be a contributing factor. Fluctuations in CBFV rather than individual readings are probably more important in the genesis of IVH. An episode of significantly reduced CBFV is a poor prognostic sign.

Clinical Pharmacology of Pinacidil, A Prototype for Drugs That Affect Potassium Channels

The clinical pharmacology of potassium channel openers has been reviewed using pinacidil as a prototype drug. When administered acutely or chronically, the hemodynamic and neuroendocrine profile is that of a peripheral arterial vasodilator. The drug produces decreases in peripheral vascular resistance, and subsequent blood pressure decreases are associated with reflex increments in heart rate. When studied, plasma catecholamines increased about twofold during chronic therapy. Plasma renin activity, however, was not increased during chronic therapy with pinacidil monotherapy. When patients were treated with pinacidil doses ranging from 12.5 to 75 mg b.i.d., 66.9% of patients had a decrease in supine diastolic blood pressure to below 91 mm Hg and 10 mm Hg less than baseline, whereas only 23.9% of patients had similar falls during placebo treatment. During maintenance therapy with pinacidil, the average blood pressure during the daytime dosing interval was 137.8 +/- 1.2/83.4 +/- 0.7 mm Hg (mean +/- SEM). Titration of pinacidil as monotherapy resulted in a characteristic adverse event profile dominated by the presence of dose-related edema. Other characteristic events included tachycardia, palpitations and headache. When pinacidil was given to patients unresponsive to hydrochlorothiazide (25 mg b.i.d.), similar efficacy relative to placebo was noted with a change of post-dose supine diastolic blood pressure in the pinacidil group of 13.5 +/- 0.8 mm Hg and 7.3 +/- 0.9 mm Hg in the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-Term Treatment of Severe Chronic Heart Failure with Captopril

Twenty-three patients with severe heart failure (NYHA classes III and IV) on treatment with digitalis and diuretics were additionally treated in a randomized double-blind study over a 6-month period with captopril (n = 12; mean daily dose 84 mg) or a placebo (n = 11) and were then reexamined. In the captopril group, the left-ventricular filling pressure decreased by 9 mm Hg (from 23 to 14) at rest and 6 mm Hg (from 35 to 29) during exercise. In the placebo group, there was an increase of 4 mm Hg (from 25 to 29) at rest and 7 mm Hg (from 33 to 40) during exercise; p less than 0.01 (p less than 0.01). In the captopril group, the cardiac index at rest increased 0.7 1/min/m2 (from 2.1 to 2.8) and during exercise 1.2 1/min/m2 (from 2.8 to 4.0). In the placebo group, the increase in cardiac index was considerably less pronounced at rest (= 0.2 1/min/m2; from 1.9 to 2.1) and during exercise (= 0.1 1/min/m2; from 2.7 to 2.8); p less than 0.02 (p less than 0.01). The improved cardiac output had a beneficial effect on the renal blood flow. Hippuran clearance increased by 46 ml/min (from 271 to 318), whereas in the control group it decreased 25 ml/min (from 259 to 234) (p less than 1.02). Both the heart rate and the arterial blood pressure remained constant, whereas the decrease in peripheral vascular resistance was definitely more pronounced in the captopril group (= 562 dyne X s X cm-5, from 1,841 to 1,279) than in the placebo group (= 123 dyne X s X cm-5, from 1,834 to 1,710; p less than 0.02). The heart volume, assessed radiographically, increased slightly in the placebo group, and the left-ventricular end-diastolic diameter remained constant in both groups. In the course of the study, two patients died in the captopril group and three in the placebo group. After six months, eight patients in the captopril group and three in the placebo group had improved by at least one NYHA category. The beneficial effects of captopril are due to its inhibitory effect on the renin-angiotensin system as well as to the inhibition of sympathetic stimulation. Consequently, in the captopril group the quantity of plasma norepinephrine decreased by 188 ng/ml (from 430 to 618); p less than 0.03. The indirect vasodilation caused by this mechanism leads to persistent unloading of the myocardium and an improvement in heart failure without loss of action by counterregulatory mechanisms.

Muscular blood flow in patients with heart failure.

We studied reactive hyperemia in a group of patients with heart failure before and after therapy, since changes in the characteristics of muscular blood flow may influence the functional class of these patients. At the same time we evaluated some echocardiographic parameters too. When the patients improved clinically, they showed an increase in muscular blood flow at rest and in percent of fractional shortening and a decrease in peripheral vascular resistance. The reactive hyperemia did not change significantly. This fact probably depends on a maximal response to the postischemic hyperemia and represents the integrity of autoregulatory mechanisms.

Vasodilators worsen gas exchange in dog oleic-acid lung injury.

The authors studied the effects of vasodilator treatment with either hydralazine or minoxidil on gas exchange and lung water accumulation over a 5-h period in canine oleic acid-induced pulmonary edema. Thirty dogs were given intravenous oleic acid 1 day prior to study to produce a stable, diffuse lung injury. On the day of study, one group of animals was given minoxidil, a potent systemic and pulmonary vasodilator. A second group was given hydralazine, a potent systemic vasodilator but weak pulmonary vasodilator, and a third group was not treated. Hemodynamic and gas exchange variables were assessed prior to treatment, and again after 5 h of treatment. Both drugs caused an increase in cardiac output and a decrease in peripheral vascular resistance. Minoxidil increased venous admixture from 17 +/- 4 to 55 +/- 6% (P less than 0.05), whereas hydralazine-treated dogs had a smaller increase, from 26 +/- 5 to 47 +/- 6% (P less than 0.05), and untreated animals did not show a significant change. Lung water increased 27 +/- 12% in the untreated animals over the course of the study, 43 +/- 18% in the hydralazine animals, and 60 +/- 16% (P less than 0.05 vs. untreated) in the minoxidil animals. The authors conclude that adverse effects may result from peripheral vasodilators in animals with permeability pulmonary edema, but the extent and severity of these effects may vary, depending on the drugs' effects on the pulmonary circulation.

Long-term results with verapamil in essential hypertension and its influence on serum lipids

Many studies have confirmed that the treatment of mild and moderate hypertension reduces mortality and morbidity from cardiovascular accidents and cardiac and renal failure; more recent studies suggest that there is some beneficial effect on ischemic heart disease. The harmful metabolic effects of some hypotensive agents on serum potassium, magnesium, uric acid, glucose, renin and lipids might reduce the beneficial effect of controlling raised blood pressure. Also, the adverse effects associated with most antihypertensive drugs have decreased quality of life and, possibly, compliance in many patients. In assessing the value of newer antihypertensive agents, other effects of the drugs must be taken into account. The calcium-channel antagonist verapamil produces a dose-dependent reduction in blood pressure with little postural effect. There is little change in heart rate and the major antihypertensive effect results from a decrease in peripheral vascular resistance, with no accompanying increase in cardiac output. In 75 patients followed for more than 1 year, tolerance to verapamil did not appear to develop, nor were there any significant changes in serum electrolytes or creatinine clearance. Fasting serum lipid levels were measured in 15 patients before and after 3 months of treatment with verapamil (80 to 160 mg, 3 times a day); there was no change in cholesterol, triglycerides or high-density lipoproteins. Verapamil is, therefore, an effective hypotensive agent with a rapid onset of action. Tolerance does not develop with prolonged use, nor does it appear to affect electrolytes or serum lipids adversely. Constipation appears to be its only limiting adverse effect.

Functional corticotropin releasing factor receptors in the primate peripheral sympathetic nervous system.

Corticotropin releasing factor (CRF) is a key hormone in the integrated response to stress, acting both as the major regulator of pituitary adrenocorticotropic hormone (ACTH) release and as a neuropeptide in the brain. The actions of CRF are mediated by specific plasma membrane receptors in the anterior pituitary gland and in discrete brain areas including the cerebral cortex and several regions related to the limbic system. In addition to the pituitary and central actions of CRF, systemic administration of the peptide in the rat, dog, monkey and man causes hypotension and tachycardia because of a decrease in peripheral vascular resistance. These observations, in conjunction with the finding of immunoreactive and bioactive CRF in peripheral tissues, suggest that the peptide is locally released in tissues to act as a neurotransmitter or paracrine hormone. As CRF is present in the adrenal medulla and the peptide is known to modulate the central activity of the autonomic nervous system, we investigated the possibility that CRF is involved in the regulation of the peripheral autonomic nervous system. Such an action of CRF is supported by our demonstration of specific CRF receptors in the monkey adrenal medulla and sympathetic ganglia. In the adrenal medulla, these receptors are coupled to adenylate cyclase and can stimulate the secretion of catecholamines and Met-enkephalin.

Cardiovascular effects of nipradilol, a beta-adrenoceptor blocker with vasodilating properties.

In anesthetized dogs, an intravenous injection of nipradilol produced a long lasting fall in mean arterial blood pressure which was accompanied by transient decreases in peripheral vascular resistance and sustained decreases in heart rate, cardiac output and left ventricular (LV) dP/dt. LV end-diastolic pressure (LVEDP) was not changed while LV diameters and central venous pressure were slightly increased. Under propranolol pretreatment conditions, nipradilol no longer affected the heart rate, but the drug still induced a transient reduction in peripheral vascular resistance, and sustained decreases in arterial blood pressure and cardiac output. Furthermore, indicators of LV preload (LVEDP, LV end-diastolic diameter and central venous pressure) were significantly reduced, suggesting a direct dilating action of nipradilol on capacitance vessels. In intact conscious dogs, nipradilol caused a sustained reduction in LVEDP, while propranolol increased LVEDP. After administration of nipradilol, coronary blood flow in anesthetized dogs decreased in association with diminished myocardial oxygen consumption, and large coronary vessel resistance also decreased. Nipradilol competitively antagonized the isoproterenol-induced positive chronotropic response (DR10: 0.04 mg/Kg, i.v.) and the phenylephrine-induced vasopressor response (DR10: 3.95 mg/Kg, i.v.). In conclusion, nipradilol, in contrast to propranolol, possesses the properties to decrease arterial blood pressure, LV preload and large coronary vessel resistance through its dilating action on arterial and venous vessels. It is proposed that nipradilol may be beneficial for the treatment of hypertension and coronary heart disease.

The immediate haemodynamic and electrophysiological response to prenalterol during fixed rate pacing in patients with chronic ischaemic heart disease.

The immediate haemodynamic and electrophysiologic effects of intravenous prenalterol 2.5-75 micrograms/kg in patients with coronary heart disease without clinical heart failure were investigated during fixed rate atrial pacing. Right ventricular peak dP/dt increased pronounced and serum concentration dependent after prenalterol concomitant with an increase in stroke volume and a moderate decrease in peripheral vascular resistance. The effects on haemodynamics after prenalterol were thus serum concentration dependent but with marked interindividual variation. AV nodal conduction velocity increased significantly. It is concluded that prenalterol possess pronounced inotropic properties. The haemodynamic response to prenalterol intravenously is to a lesser degree dependent on the chronotropic effects of the drug and it is often unpredictable.

Rationale for calcium entry-blocking drugs in systemic hypertension complicated by coronary artery disease

There is considerable rationale for the use of the calcium entry-blocking drugs for the treatment of hypertension and prevention of recurrent episodes of angina pectoris in patients with systemic hypertension and significant coronary artery disease—the 2 entities commonly occurring together. Calcium entry-blocking drugs improve myocardial blood flow while decreasing myocardial oxygen demand. These agents can be given to most patients with ischemic heart disease and its complications, and are associated with a relatively low incidence of serious adverse effects and toxicity during long-term therapy. They reduce the frequency of anginal attacks, prolong exercise time to ST-segment depression or angina and improve exercise capacity. With long-term therapy, tolerance does not develop as it does in many patients with the “long-acting” nitrates. Calcium entry-blocking drugs reduce systolic blood pressure in patients with hypertension by a decrease in peripheral vascular resistance and a uniform improvement in blood flow affecting the myocardium, kidney and brain. There are no central nervous system adverse effects and hypokalemia does not occur. Unlike therapy with the β-blocking drugs, chronic treatment with the calcium entry blockers does not reduce the serum level of high-density lipoprotein cholesterol nor increase serum triglyceride concentration. The calcium blockers decrease the arterial blood pressure without increasing intravascular plasma volume and are associated with only a slight increase in reflex-mediated sympathetic activity and heart rate, the latter occurring predominantly with nifedipine. Calcium entry-blocking drugs provide alternative or preferred therapy to β-blocking agents in patients with a combination of hypertension and angina pectoris. They are likely to be more effective in elderly patients and in blacks and can be prescribed for patients with bronchospastic disease and symptomatic peripheral vascular disease. For many reasons, of the 3 currently available calcium blockers, dilatizem is likely to be the most effective calcium entry blocker for monotherapy In patients with hypertension and ischemic heart disease, although most worldwide experience for this indication has been with nifedipine.

Cardiovascular and endocrine effects of potassium in spontaneously hypertensive rats.

Although potassium is known to lower blood pressure in a number of forms of experimental and human hypertension, the mechanism for this effect remains unclear. We studied several possible mechanisms for this effect in the spontaneously hypertensive rat (SHR). Fourteen-week-old SHR were given 0.5% KCl in the drinking water. This potassium supplement resulted in a 16-mmHg fall in mean arterial pressure and a 22% decrease in peripheral vascular resistance. Plasma potassium increased 0.4 meq/l, while muscle potassium was unchanged. Potassium supplementation resulted in no change in plasma renin activity, plasma aldosterone, or plasma norepinephrine. Urinary excretion of prostaglandin (PG) E2 and 6-keto-PGF1 alpha was also not altered by potassium supplementation. Potassium-supplemented SHR were found to have no difference in sodium excretion compared with control SHR, and plasma volume was similar in both groups. The pressor response to angiotensin II and norepinephrine was not substantially affected by potassium supplementation. Furthermore, baroreflex control of heart rate was not altered by potassium supplementation. Finally, potassium supplementation resulted in no change in mesenteric artery angiotensin II receptor number or receptor affinity. Therefore, although potassium lowers blood pressure in the SHR by decreasing peripheral vascular resistance, the mechanism of this effect on vascular resistance remains unknown.

The acute haemodynamic effects of oral nicardipine.

The haemodynamic effects of oral nicardipine at two different doses were assessed in fifteen patients at rest following diagnostic cardiac catheterisation. Six patients received four doses of 20 mg nicardipine hydrochloride orally every 8 h, and nine patients received four doses of 30 mg orally every 8 h. No side effects were encountered with either dose. At both dose levels, there was a significant fall in systemic vascular resistance, significant increases in heart rate and cardiac output, and no change in stroke volume index. No changes were seen in pulmonary vascular haemodynamics, and there were no significant changes in mean arterial pressure. Plasma levels of nicardipine reached a peak within 1 h. In parallel with the haemodynamic effects, the plasma concentrations achieved after the third and fourth doses were higher than after the first dose. These haemodynamic changes are consistent with a vasodilator effect, which produces a decrease in peripheral vascular resistance. It would appear that the 30 mg dose has a more potent vasodilator action than the 20 mg dose and, in the patients studied, this larger dose was not associated with any side effects.

Calcium in the pathogenesis and therapy of human hypertension

The contribution of calcium to normal regulation of blood pressure is reviewed. Epidemiologic data suggest that abnormal calcium homeostasis may play a role in dietary and environmental contributions to the risk of hypertension and cardiovascular disease. Recent studies in human and experimental hypertension point to one or more defects in cellular handling of calcium as contributing to the initiation and maintenance of increased vascular tone and, thereby, to abnormally elevated arterial blood pressure. By “correcting” some of these defects, calcium channel blockers may represent relatively specific therapy for hypertension. Data from human trials are still limited, but it is evident that, following oral administration of nifedipine and related compounds, an immediate decrease in peripheral vascular resistance and mean arterial pressure is produced. Cardiac output is not altered, and renal perfusion is maintained. In contrast to many currently used antihypertensive agents—including thiazide diuretics and beta blockers—which frequently Induce alterations in the patient's serum chemical values, long-term administration of calcium channel blockers does not produce significant adverse metabolic effects or substantive changes in biochemical parameters.

Controlled hypotension with adenosine in cerebral aneurysm surgery.

The cardiovascular effects of adenosine-induced controlled hypotension were studied in 10 patients undergoing cerebral aneurysm surgery. Adenosine and its metabolites were measured in arterial plasma using high-pressure liquid chromatography. Whole body and cerebral arteriovenous oxygen content differences (AVDO2), arterial lactate levels, and arteriojugular lactate differences were determined. In order to reduce the dose requirement of adenosine, the patients were pretreated with the adenosine uptake inhibitor, dipyridamole (0.3-0.4 mg . kg-1). During the infusion of adenosine (0.14 +/- 0.04 mg . kg-1 . min-1) the mean arterial blood pressure decreased by 43%, from 82 to 46 mmHg, during a mean hypotensive period of 32 min, without signs of tachyphylaxis. The arterial adenosine level increased from 0.15 +/- 0.02 to 2.45 +/- 0.65 microM (P less than 0.01). Hypotension was caused by a profound decrease in peripheral vascular resistance (61 +/- 3%, P less than 0.01), which was accompanied by an increase in cardiac output (44 +/- 9%, P less than 0.01). Heart rate increased moderately by 16 +/- 5% (P less than 0.01). Pulmonary vascular resistance and central venous pressures were unaffected. Arterial lactate and PaO2 were unchanged, while whole body oxygen consumption was decreased by 13 +/- 4% (P less than 0.05). The AVDO2 across the brain was decreased by 37 +/- 5% (P less than 0.05) without signs of lactate formation. The authors conclude that adenosine rapidly induces a stable and easily controlled hypotension in humans by dilation of arterial resistance vasculature.

The dopamine agonist bromocriptine induces hypotension by venous and arteriolar dilation.

Acute bromocriptine administration reduced sitting and standing blood pressure and produced severe orthostatic hypotension in 12 normal subjects. Concomitantly, there was an increase in venous distensibility and basal blood flow, and a decrease in peripheral vascular resistance, as determined by forearm plethysmography. After administration of bromocriptine, plasma norepinephrine concentration decreased. Bromocriptine lowers blood pressure by dilating arterioles and veins, at least in part by means of dopaminergic inhibition of sympathetic nervous system activity.

Role of angiotensin II, alpha-adrenergic system, and arginine vasopressin on arterial pressure in rat.

Three pressor systems regulate arterial pressure (MAP): angiotensin II (ANG II), the alpha-adrenergic system, and arginine vasopressin (AVP). In this study we determined the ability of each system to support MAP in the conscious rat when the other two systems were inactivated. After administration of the converting-enzyme inhibitor teprotide (CEI) and the alpha-adrenergic receptor antagonist phenoxybenzamine (POB), MAP decreased 40% as a result of a 45% decrease in peripheral vascular resistance (PVR). Despite hypotension, plasma AVP levels were not increased, and an AVP pressor antagonist (AVP-A) did not result in a further decrease in MAP. Thus the profound hypotension after POB plus CEI was the result of inhibition of all three systems. POB, rather than CEI, prevented AVP release since following hypotensive hemorrhage, plasma levels reached 51 +/- 13 pg/ml with CEI but only 4.7 +/- 0.8 pg/ml with POB. To study the pressor effect of AVP alone, AVP was infused in POB plus CEI-treated rats. AVP increased MAP (from 68 +/- 4 to 92 +/- 5 mmHg; P less than 0.005) and plasma AVP (to 13.8 +/- 1.9 pg/ml). Since POB inhibited both the AVP and the alpha-adrenergic system, the role of ANG II alone was determined in POB-treated rats. In the presence of ANG II MAP was 97 +/- 1 mmHg. To study the alpha-adrenergic system, MAP was determined in CEI plus AVP-A-treated rats. In the presence of an intact alpha-adrenergic system MAP was 101 +/- 1 mmHg. We conclude that PVR and MAP are profoundly decreased in the absence of all three pressor systems.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of hypertension and captopril on the cataractogenesis in SHRSP studied by electron microscopic observation of ciliary body

As reported previously, captopril has an antihypertensive effect and suppresses the appearance and progression of sclerotic changes in the retinal arteriolar wall. This effect of captopril are probably brought by decrease of peripheral vascular resistance (Acta Soc. Ophthalmol. Jpn. 86: 227-238, 1982). Vascular lesions caused by sustained hypertension have been also confirmed in the tributaries of long posterior ciliary artery in SHRSP rats (Folia ophthalmol. Jpn. 30: 1907-1918, 1979).The present study revealed that degenerative lesions occurred in the epithelia and blood vessels of ciliary body which has been thought to be responsible for the production of aqueous humor and for the nutrition of the crystalline lens. The lesions were more severe in the animal of poor controlled high blood pressure, at least in SHRSP, in accordance with the severity of cataract.The lesions found in the ciliary body of SHRSP were probably induced by a damage of aqueous barrier following tissue ischemia as the hypertensive complication in the tributaries of long posterior ciliary artery. These findings might be a clue for the resolution of pathogenesis of human senile cataract.