Diuretic herb Gomphrena celosioides Mart. (Amaranthaceae) promotes sustained arterial pressure reduction and protection from cardiac remodeling on rats with renovascular hypertension.

ETHNOPHARMACOLOGICAL RELEVANCE: Gomphrena celosioides Mart., belonging to the Amaranthaceae family, is a weed known as "perpétua," and its ethnopharmacological use is to treat of urinary tract disorders and kidney stones. Urinary tract disorders and kidney stones could include several pathological conditions such hypertension, diuretic and lithiasic problems. In the present work a model of renovascular hypertension was developed in vivo to investigate its usefulness as an antihypertensive drug. AIM OF THE STUDY: Evaluate the effect of acute and 28 day oral administration of G. celosioides extract on systemic arterial pressure and diuresis of renovascular-hypertensive rats, as well as its effect on cardiac remodeling and vascular reactivity. MATERIALS AND METHODS: Ethanolic extract of G. celosioides (EEGC) was used. To induce renovascular hypertension, adult male Wistar rats were submitted to Goldblatt 1K1C or 2K1C surgery. The mean arterial pressure (MAP) of 1K1C animals was directly assessed by cannulation of the carotid artery before and after intraduodenal acute administration of 30, 100 or 300 mg/kg of EEGC. For the 4-week assay, 2K1C animals received daily treatments with water (control group), 100 mg/kg EEGC or 15 mg/kg enalapril for 28 days. Diuresis and caudal blood pressure were assessed weekly, and at the 28th day of treatment, the MAP was directly quantified shortly before euthanasia. Internal organs were removed, weighed and routinely processed for histology and the left ventricle wall was measured. Blood was collected for biochemical analysis and mechanism investigation by quantification of angiotensin converting enzyme (ACE) activity and aldosterone, nitrite and thiobarbituric acid reactive substances (TBARS) concentration. The rats' mesenteric beds were isolated and cannulated to have their pressure variation assessed after crescent doses of phenylephrine (Phe), acetylcholine (ACh) and sodium nitroprusside (SNP). RESULTS: EEGC acutely reduced MAP the dose of 100 mg/kg. In the 4-week assay, EEGC acted as diuretic after acute administration after 1, 2, 3 and 4 weeks of treatment. EEGC also acted as an antihypertensive and it showed significant difference already after 1 week (and after 3 and 4 weeks) compared to control, with its MAP close to pre-surgery values at the end of the experiment. It promoted ACE inhibition, which led to lower aldosterone levels. The lower TBARS and higher nitrite concentration found in the EEGC group suggest antioxidant activity and NO maintenance. Moreover, EEGC counteracted the impairment of vascular reactivity induced by renovascular hypertension. The extract group presented thinner left ventricle wall compared to the control, meaning reduced hypertension-induced cardiac remodeling. CONCLUSIONS: The G. celosioides diuretic effect is maintained on renovascular hypertensive rats and can reduce the blood pressure after the first week of treatment by inhibiting ACE and these effects are longstanding and strong enough to promote protection against cardiac remodeling. Therefore, it shows potential as an antihypertensive drug.

Direct renin inhibition is not enough to prevent reactive oxygen species generation and vascular dysfunction in renovascular hypertension.

Renin-angiotensin system activation promotes oxidative stress and endothelial dysfunction. However, no previous study has examined the effects of the renin inhibitor aliskiren, either alone or combined with angiotensin II type 1 antagonists on alterations induced by two-kidney, one-clip (2K1C) hypertension. We compared the vascular effects of aliskiren (50mg/kg/day), losartan (10mg/kg/day), or both by gavage for 4 weeks in 2K1C and control rats. Treatment with losartan, aliskiren, or both exerted similar antihypertensive effects. Aliskiren lowered plasma Ang I concentrations in sham rats and in hypertensive rats treated with aliskiren or with both drugs. Aliskiren alone or combined with losartan decreased plasma angiotensin II concentrations measured by high performance liquid chromatography, whereas losartan alone had no effects. In contrast, losartan alone or combined with aliskiren abolished hypertension-induced increases in aortic angiotensin II concentrations, whereas aliskiren alone exerted no such effects. While hypertension enhanced aortic oxidative stress assessed by dihydroethidium fluorescence and by lucigenin chemiluminescence, losartan alone or combined with aliskiren, but not aliskiren alone, abolished this alteration. Hypertension impaired aortic relaxation induced by acetylcholine, and losartan alone or combined with aliskiren, but not aliskiren alone, reversed this alteration. Losartan alone or combined with aliskiren, but not aliskiren alone, increased plasma nitrite concentrations in 2K1C rats. These findings show that antihypertensive effects of aliskiren do not prevent hypertension-induced vascular oxidative stress and endothelial dysfunction. These findings contrast those found with losartan and suggest that renin inhibition is not enough to prevent hypertension-induced impaired redox biology and vascular dysfunction.

Aqueous extract of dioscorea opposita thunb. normalizes the hypertension in 2K1C hypertensive rats.

BACKGROUND: Dioscorea opposita Thunb. (Huai Shan Yao, DOT), a common staple food in China, has been used for more than 2000 years in traditional Chinese medicine (TCM) to treat different systemic diseases including hypertension. The objective of this study was to investigate the possible antihypertensive effects of the aqueous extract of (DOT) in renovascular hypertensive rats as well as the mechanism in reducing blood pressure. METHODS: The two-kidney one-clip (2K1C) Goldblatt model of renovascular hypertension was used in Wistar rats. Rats with captopril, low-dose DOT and high-dose DOT treated 2K1C groups for 6 weeks. The blood pressure, cardiac mass index (heart weight/body weight), plasma level of angiotensin-II (Ang-II), endothelin-1(ET-1), superoxide dismutase (SOD) and malondialdehyde (MDA) were evaluated. RESULTS: DOT significantly reduced mean systolic and diastolic blood pressure after treatment. DOT also significantly increased plasma SOD activity but decreased plasma MDA concentration. Renal function was improved with captopril and DOT. DOT reduced plasma Ang-II activity and plasma ET concentration. They couldalso significantly reduce the left ventricular hypertrophy and cardiac mass index. CONCLUSIONS: Our results suggest that DOT may have an antihypertensive effect on hypertension by inhibit ET-converting enzyme and antioxidant activity, which warrant further exploration.

Cimicifuga racemosa impairs fatty acid ß-oxidation and induces oxidative stress in livers of ovariectomized rats with renovascular hypertension.

The aim of this work was to evaluate the effects of therapeutic doses of Cimicifuga racemosa on cardiovascular parameters and on liver lipid metabolism and redox status in an animal model of estrogen deficiency associated with hypertension, a condition that could make the liver more vulnerable to drug-induced injuries. Female Wistar rats were subjected to the surgical procedures of bilateral ovariectomy (OVX) and induction of renovascular hypertension (two-kidneys, one-clip; 2K1C). These animals (OVX + 2K1C) were treated with daily doses of a C. racemosa extract, using a dose that is similar to that recommended to postmenopausal women (0.6 mg/kg), over a period of 15 days. The results were compared to those of untreated OVX + 2K1C, OVX, and control rats. The treatment with C. racemosa caused a significant reduction in blood pressure. In the liver, treatment did not prevent the development of steatosis, and it reduced the mitochondrial and peroxisomal capacity to oxidize octanoyl-CoA compared to the untreated animals. In addition, C. racemosa caused numerous undesirable effects on the liver redox status: it increased the mitochondrial reactive oxygen species generation, an event that was not accompanied by an increase in the activity of superoxide dismutase, and it induced a decrease in peroxisomal catalase activity. Although the reduced glutathione content had not been affected, a phenomenon that probably reflected the restoration of glucose-6-phosphate dehydrogenase activity by C. racemosa, oxidative damage was evidenced by the elevated level of thiobarbituric acid-reactive substances found in the liver of treated animals.

Antihypertensive effect of long-term oral administration of jellyfish (Rhopilema esculentum) collagen peptides on renovascular hypertension.

Antihypertensive effect of long-term oral administration of jellyfish (Rhopilema esculentum) collagen peptides (JCP) on renovascular hypertension rats (RVHs) was evaluated. The systolic blood pressure and diastolic blood pressure of the RVHs were significantly reduced with administration of JCP (p < 0.05), compared with model control group. However, the arterial blood pressure of normal rats showed no significant changes during long-term oral treatment with high dose JCP (p > 0.05). Furthermore, effect of JCP on angiotensin II (Ang II) concentration of plasma had no significance (p > 0.05), but JCP significantly inhibited the Ang II concentration in RVHs' kidney (p < 0.05). The kidney should be the target site of JCP.

Renal artery stenosis in kidney transplants: assessment of the risk factors.

BACKGROUND: Transplant renal artery stenosis (TRAS) is an important cause of hypertension and renal allograft dysfunction occurring in kidney transplant recipients. However, conflicting predisposing risk factors for TRAS have been reported in the literature. OBJECTIVE: The aim of the present study was to assess the potential correlation between possible risk factors and TRAS in a group of living donor renal transplant recipients 1 year after the renal transplantation. METHODS: We evaluated the presence of renal artery stenosis in 16 recipients who presented with refractory hypertension and/or allograft dysfunction 1 year after renal transplantation. Screening for TRAS was made by magnetic resonance angiography and diagnosis was confirmed by conventional renal angiography. Age, gender, history of acute rejection, plasma lipid profile, serum creatinine, blood urea nitrogen, serum uric acid, calcium phosphate (CaPO4) product, alkaline phosphatase, fasting blood sugar, hemoglobin, and albumin were compared between the TRAS and non-TRAS groups. RESULTS: Of 16 kidney transplant recipients, TRAS was diagnosed in three patients (two men and one woman). High levels of calcium, phosphorous, CaPO4 product, and low-density lipoprotein (LDL) cholesterol were significantly correlated with the risk of TRAS 1 year after renal transplantation (P < 0.05). Serum level of uric acid tended to have a significant correlation (P = 0.051). CONCLUSION: Correlation between high CaPO4 product, LDL cholesterol, and perhaps uric acid and TRAS in living donor renal transplant recipients 1 year after renal transplantation might suggest the importance of early detection and tight control of these potential risk factors.

[Influence of Tiangou Jiangya capsule on blood pressure in renovascular hypertension rats].

OBJECTIVE: To observe the effect of Tiangou Jiangya capsule (TJC) on blood pressure in renovascular hypertension rats and explore its possible mechanism. METHOD: Seventy-two Wistar rats were randomly divided into normal control group, model group, captopril group, TJC small, medium and high dose groups. Non-invasive blood pressure measurement was used to detect the arterial blood pressure of rat tails. PRA, Ang II , ALD, 6-Keto-PGF1alpha, ET and TXB2 content in blood was measured by radioimmunoassay. NO content in blood was determined by method of nitrate reductase. RESULT: The systolic, diastolic and mean pressure significantly increased, serum PRA, Ang II , ALD decreased, ET levels significantly increased in model group rats. TJC significantly reduced blood pressure, improved the plasma renin activity, decreased ET levels and increased NO content of model rats. CONCLUSION: TJC can reduce blood pressure of renovascular hypertention rats, and the mechanism may be related to its regulating lower blood pressure regulation of the secretion of RAAS system and improving vascular endothelial function.

Quercetin restores plasma nitrite and nitroso species levels in renovascular hypertension.

Quercetin has antioxidants properties which may increase nitric oxide (NO) bioavailability. However, the effects of quercetin on NO status have been poorly studied. We evaluated whether quercetin improves the plasma levels of NO metabolites in two-kidney one-clip (2K1C) hypertensive rats and assessed its effect on endothelial function. Sham-operated and 2K1C rats were treated with quercetin (10 mg(-1) kg(-1) day(-1) by gavage) or vehicle for 3 weeks. Systolic blood pressure (SBP) was monitored weekly. Vascular responses to acetylcholine (Ach) and sodium nitroprusside (SNP) were assessed in hindquarter vascular bed. Plasma nitrate levels were assessed by Griess reagent and plasma nitrite and nitroso species (S, N-nitroso species) were assessed by ozone- based chemiluminescence. Aortic NADPH oxidase activity and superoxide production were evaluated. While quercetin had no effects in control normotensive rats (P > 0.05), it significantly reduced SBP in 2K1C rats (P < 0.05). At the end of treatment, plasma nitrate levels were similar in all experimental groups (P > 0.05). However, plasma nitrite and the nitroso species levels were significantly lower in 2K1C rats when compared with controls (P < 0.05). Quercetin treatment restored plasma nitrite and nitroso species levels to those found in the sham-vehicle group (P < 0.05). While quercetin treatment induced no significant changes in responses to SNP (P > 0.05), it restored the vascular responses to Ach. Quercetin significantly attenuated 2K1C-hypertension-induced increases in NADPH oxidase activity and vascular superoxide production (P < 0.05). These results suggest that the antihypertensive effects of quercetin were associated with increased NO formation and improved endothelial function, which probably result from its antioxidant effects.

[Effects of sapindoside on blood pressure and vasoactive substance in renovascular hypertension rat].

OBJECTIVE: To observe the effects of sapindoside on blood pressure, Ang II, Ald, ET in the blood plasma and NO in the serum in renovascular hypertension rat. METHOD: The 2K1C (2 kidney 1 clap) hypertensive model rats were used and drugs had been given by ig. for 5 weeks. The blood pressure was measured at the 1, 3, 7, 14, 21, 28, 35 day after drug. At the end of 5th weeks, the Ang II, Ald, ET in the blood plasma and NO in the serum were measured. RESULT: Sapindoside (H, M and L) by ig. for 5 weeks could significantly lower the blood pressure, increase the levels of NO in the serum, reduce the concentration of Ang II, Ald, ET in the blood plasma. CONCLUSION: Sapindoside plays an important role in decreasing the blood pressure of renovascular hypertension rat.

[Effects of Peristrophe roxburghiana on blood pressure. NO and ET in renal hypertensive rats].

OBJECTIVE: To observe the effects of Peristrophe roxbrughiana (HSX) on blood pressure, NO, No-synthase and ET in the serum and NO in urine in renal hypertensive rats. METHODS: The 2K1C(2 kidney 1 clap) hypertensive model rats were used and drugs had been given by ig. for 4 weeks. The blood pressure was measured at the end of the each week. At the end of 4th week, the urine was collected and the concentration of NO in the serum or urine, NO-synthease and ET in the serum were measured. RESULTS: HSX (H or L dosage) by ig. for 1 week can significantly lower the blood pressure, increase the levels of NO and NO-synthase in the serum and NO in the urine, reduce the concentration of ET in the serum. The effects have lasted for 4 weeks. CONCLUSION: HSX played an important role in the renal hypertensive rats.

Hypercholesterolemia and hypertension have synergistic deleterious effects on coronary endothelial function.

OBJECTIVE: Coronary endothelial dysfunction is associated with an increase in cardiac events. Hypercholesterolemia (HC) and hypertension (HT) are both associated with endothelial dysfunction, and their coexistence is associated with an increased incidence of cardiac events in epidemiological studies. However, pathogenic mechanisms are poorly understood. Here we studied the effects of coexisting HC and HT on coronary endothelial function. METHODS AND RESULTS: Four groups of pigs were studied after 12 weeks of a normal diet (n=9), a 2% HC diet (n=9), HT (achieved by unilateral renal artery stenosis, n=8), or HC+HT (n=6). Coronary endothelial function was tested, in epicardial arteries and arterioles, by using organ chamber techniques. Oxidative stress was measured in coronary artery tissue. Vasodilatory response to bradykinin and calcium ionophore was significantly impaired in animals with HC+HT compared with each risk factor alone (P<0.05 for both). In animals with coexistent HC and HT, the increase in oxidative stress was more pronounced compared with each risk factor alone (P<0.05). Furthermore, chronic antioxidant supplementation significantly improved coronary artery vasoreactivity. CONCLUSIONS: These results suggest that HC and HT have a synergistic deleterious effect on coronary endothelial function, associated with increased oxidative stress. This interaction may contribute to the increased incidence of coronary heart disease and cardiac events seen when HC and HT coexist.

[Effect of xueling on relating substances of renal hypertension in rats].

Xueling(p.o.) obviously reduces the aldosterone content of renal hypertension rats, but not affecting markedly the endothelin, atrial natriuretic factor, calcitonin gene-related peptide, thromboxane B2 and 6-keto-prostaglandin F1 alpha. The content reduction of aldosterone is one of the mechanisms to lower blood pressure.

[Effects of acupuncture on blood pressure, SOD,LPO and five kinds of trace elements to stenosis of renal artery caused hypertension in rats].

Changes of blood pressure, superoxide dismutase (SOD), lipid peroxidation (LPO) and concentration of five kinds of trace elements including Cu, Zn, Fe, Ca, Mg were observed before or after acupuncture treatment in the stenosis of renal artery caused hypertension in rats [correction of mice]. It was demonstrated that acupuncture in the points of Zusanli, Neiguan, Sanyinjiao and Yongquan in mice could reduce the blood pressure significantly and influence the concentrations of SOD, LPO and five kinds of trace elements in the stenosis of renal artery caused hypertension in mice. The possible mechanisms of acupuncture in reducing the blood pressure and influencing the changes of SOD, LPO and five kinds of trace elements were also discussed.

Effects of acupuncture on blood pressure and plasma renin activity in two-kidney one clip Goldblatt hypertensive rats.

Shih-Hsüan [Sipseon (EX-UE-11)] are Curious loci lying outside of the meridians on the tips of each finger. These loci have long been the acupuncture sites for the treatment of cardiovascular disease in oriental medicine. Alterations in the renin-angiotensin system have been considered as the pathophysiological basis of the origin and/or maintenance of hypertension. Activation of the plasma or tissue renin-angiotensin system may be one of the cause of hypertension. The aim of the present study was to elucidate the effects of acupuncture on blood pressure and plasma renin activity. Acupuncture was applied on the EX-UE-11 of two-kidney one clip Goldblatt hypertensive rats. Both the systolic blood pressure and the plasma renin activity decreased significantly after treatment with acupuncture on the EX-UE-11. In the sham-operated and control rats, the procedure influenced the parameters without significant changes. The results suggest that the suppressive hemodynamic effect of acupuncture on the EX-UE-11 may be related to changes in plasma renin activity.

[The effect of heparin in vasorenal hypertension on blood electrolyte balance, on the abdominal aortic walls and on the erythrocyte rheological properties in rats]. / Vliianie geparina pri vazorenal'noi gipertenzii na balans élektrolitov krovi i stenki briushnoi aorty i reologicheskie svoistva éritrotstov krys.

The paper provides the results of experimental studies of the effects of heparin given to albino rats with vasorenal hypertension in a dose of 150 U/kg on electrolyte levels in plasma, erythrocytes, cardiac and abdominal aortic tissues, the viscosity coefficient and charge of erythrocytic suspension, transmural difference of abdominal aortic potentials. Heparin has been shown to correct hypertension-induced changes in the transmural difference of abdominal aortic potentials, the charge and viscosity coefficient of erythrocytic suspension, the gradient of sodium, potassium, and calcium in the system of erythrocyte-plasma-abdominal aortic wall.

[The effect of heparin in vasorenal hypertension on the rheological properties of the erythrocytes and on the electrolyte balance of the blood and of the wall of the abdominal aorta]. / Vliianie geparina pri vazorenal'noi gipertenzii na reologicheskie svoistva éritrotsitov, balans élektrolitov krovi i stenki briushnoi aorty.

In hypertension there was shown an increase of the erythrocyte suspension viscosity coefficient, a decrease of the transmural difference of the abdominal aorta potentials and the erythrocyte charge at a lowering of the level of the studied electrolytes in plasma, the abdominal aorta wall and an increase of sodium content in erythrocytes. Heparin corrected the changes in the coefficient of viscosity and charge of erythrocytes, the transmural difference of potentials, potassium and magnesium levels in erythrocytes, sodium level in the abdominal aorta wall induced by hypertension. On the whole there was observed no levelling by heparin of electrolyte imbalance in the erythrocyte-plasma-abdominal aorta wall system.

[Circulatory and renin response to the administration of nifedipine in renovascular hypertension]. / Risposta circolatoria e reninica alla somministrazione di nifedipina nella ipertensione renovascolare.

In 12 severe (diastolic values averaging 114 mmHg) hypertensives with unilateral renal artery stenosis (angiography) and hyperreninemia, we investigated the acute effects of nifedipine (10 mg orally) on renin and systemic hemodynamics. Plasma renin activity was determined on blood samples withdrawn from the aorta and both renal veins, so that "ischemic lateralization" could be evaluated through appropriated derived indexes. Nifedipine promptly and significantly lowered the aortic pressure in all patients. At 30 min maximal circulatory responses were recorded, which consisted of 22% decrease in mean aortic pressure (from an average of 144.6 +/- 15 to an average of 113 +/- 11 mm Hg), 44% reduction of systemic vascular resistance (from 2162 +/- 540 to 1205 +/- 279 dynes.S.cm-5), 33% rise of cardiac index (from 2920 +/- 970 to 3875 +/- 986 ml/min/m2). These effects were still evident, although somewhat tempered, after 180 min continuous monitoring; they were qualitatively and quantitatively similar to those reported by some authors in primary hypertensives with similar levels of blood pressure. After nifedipine, renin activity of the systemic blood significantly rose, due to a potentiated release from the kidney with arterial stenosis. This effect, that was interfered as a due to further reduction of the renal perfusion pressure, improved the significance of "ischemic lateralization" indexes and supported the diagnosis of renovascular hypertension in all of cases. It is suggested that nifedipine may not only be regarded as an additional diagnostic tool, but also as an effective antihypertensive agent in this disorder, al least in the short term. This contrasts with the previous suggestion of nifedipine as substantially more effective in low-renin rather than high-renin hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effect of antiadrenergic and myotropic hypotensive agents on the blood kallikrein-kinin system in experimental hypertension]. / Vliianie antiadrenergicheskikh i miotropnykh gipotenzivnykh sredstv na kallikrein-kininovuiu sistemu krovi pri éksperimental'noi gipertenzii.

In the period of vasorenal hypertension formation in rats phase changes in the kallikrein-kinin system of the blood are observed: one month after kidney-skin anastomosis a significant increase of the levels of prekallikrein, kininogen and kallikrein inhibitor is noted and by the end of the second month a drastic decrease of the levels of these components occurs due to the "unregulated" activation of the kallikrein-kinin system of the blood. Antiadrenergic agents (reserpine, tropaphen) prescribed for treatment of hypertension prevent the development of the "unregulated" activation of the kallikrein-kinin system and reduce consumption of its components. These drugs are advisable to use under threat of the kallikrein-kinin system exhaustion. beta-adrenoblocking agent obsidan and myotropic drugs produce a significant enhancement of kallikreino- and kininogenesis, but the degree of activation of the processes is less pronounced than in untreated hypertensive rats.

Hypertension and atherosclerosis in cholesterol-fed rabbits. II. One-kidney, one clip Goldblatt hypertension treated with nifedipine.

Eight groups of New Zealand white rabbits were used to study the effects of moderate chronic one-kidney, one clip hypertension (HT) and long-term nifedipine therapy on atherogenesis. Four groups were fed a normal diet (ND) over an 8-month study period; two groups, one of which was given nifedipine, remained normotensive (NT) throughout the study. Of the two HT groups, one remained hypertensive for 7 months; the blood pressure of the other group was normalized after 2 months with nifedipine. The other four groups of animals were similarly constructed except that they were fed a 0.1% cholesterol diet (CD). The results showed that: although scattered fibromuscular vascular lesions were present in the aortas of normal-diet, HT animals no atheroma was observed; neither moderate chronic HT nor abrupt, short-term HT exacerbated atherogenesis in the CD-animals; nifedipine therapy had no suppressive effect on either fibromuscular lesions or atherogenesis; nifedipine therapy reduced the aorta weight of the normotensive ND and CD groups; the aortic triglyceride content of both dietary groups was reduced by nifedipine; cholesterol content was unaffected; left ventricular hypertrophy was evident only in HT-untreated groups; and only the weight of the left ventricle of the ND-NT-treated group was significantly reduced, but the mitochondria volume per unit volume of left ventricle myocardial cells was reduced only in the NT-CD group treated with nifedipine. It is concluded that an antihypertensive dosage of nifedipine administered to animals with atherosclerosis does not suppress subsequent atherogenesis.

Antihypertensive and aldosterone-lowering effects of synthetic atrial natriuretic factor in renin-dependent renovascular hypertension.

A 24-amino acid residue synthetic atrial natriuretic factor (ANF) antagonizes angiotensin II-induced vascular contractility and aldosterone production in isolated blood vessels and adrenal cells, respectively. To determine the significance of these effects in vivo, the blood pressure and aldosterone responses to synthetic ANF were evaluated in rats with two-kidney, one clip hypertension (n = 5) and in sham-operated controls (n = 4). In the latter, ANF caused a slight fall in mean blood pressure (-7 +/- 3%) and inconsistent changes in plasma renin and aldosterone. In hypertensive rats, ANF decreased blood pressure by 31 +/- 7 mmHg (17 +/- 3%), comparable to the effect of the angiotensin antagonist saralasin (31 +/- 4 mmHg). Plasma renin activity increased from 48 +/- 15 to 79 +/- 23 ng/ml/h. Despite this, ANF caused marked suppression of plasma aldosterone (from 97 +/- 28 to 20 +/- 8.9 ng/100 ml). These results show that ANF can exert potent antihypertensive and aldosterone-lowering effects in vivo, at least when the renin-angiotensin system is stimulated.