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S Sesoko

Publications and source records attributed to S Sesoko.

31 records · Page 2Linked to original sources
PubMed1987

Predisposing factors for the development of malignant essential hypertension.

To clarify predisposing factors for malignant hypertension, we retrospectively investigated the histories of 39 patients with malignant hypertension and 39 patients with benign hypertension. Between the malignant and benign groups, there was a statistically significant difference in blood pressure but not in age when hypertension was first noticed. The number of patients who had discontinued drug treatment was significantly greater in the malignant group (19; 49%) than in the benign group (11; 28%). Insufficient sleep, overwork, and/or mental burden of long duration were factors noticed within one year before the occurrence of the malignant phase in 11 (37%) of the 30 patients in that group in whom this information was available. Patients in the malignant group tended to belong to a lower social class. These results suggest that severe hypertension from an early phase, interruption of drug treatment, and physical and/or mental burden may predispose to the development of malignant hypertension, and that these predisposing factors are likely to be associated with social class.

Adult↗
PubMed1985

Cough associated with the use of captopril.

Captopril is an orally active angiotensin-converting enzyme inhibitor that has been widely used in treating hypertension. We present a case of cough associated with captopril treatment in a patient with essential hypertension.

Aged↗
PubMed1984

Reduced cardiac mass by nitrendipine is dissociated from systemic or regional haemodynamic changes in rats.

The effects of prolonged treatment (3 weeks) with nitrendipine (10 mg X kg-1 twice daily) on systemic and regional haemodynamics and cardiac mass were studied in SHR and WKY rats. Nitrendipine markedly decreased mean arterial pressure (26.0 +/- 0.4 vs 19.9 +/- 0.6 kPa, P less than 0.01) and total peripheral resistance (0.090 +/- 0.004 vs 0.066 +/- 0.004 U X kg-1, P less than 0.01) in SHR without significantly affecting cardiac output and heart rate, whereas in the WKY rats no significant systemic haemodynamic changes were noted. Increased splanchnic blood flow and a reduced splanchnic vascular resistance were found in the WKY rats; however, in the SHR rats, blood flows (ml X min-1 X g tissue-1) increased and organ vascular resistances (kPa X ml-1 X min-1 X 100 g tissue-1) decreased significantly (P less than 0.01) in the heart (5.25 +/- 0.28 vs 7.27 +/- 0.31 and 0.04 +/- 0.00 vs 0.02 +/- 0.00; P less than 0.01) and kidneys (6.53 +/- 0.4 vs 7.98 +/- 0.2 and 0.03 +/- 0.00 vs 0.02 +/- 0.00; P less than 0.01), respectively. Nevertheless, in both rat strains, absolute cardiac mass and left ventricular weight were reduced; but in the SHR rats, the relative weight of the heart and left ventricle to body weight was also reduced significantly (3.79 +/- 0.06 vs 3.31 +/- 0.09; P less than 0.01 and 2.85 +/- 0.06 vs 2.70 +/- 0.06; P less than 0.01, respectively). Thus, these studies show that nitrendipine, a slow-entry channel calcium blocker, regressed cardiac mass in rats through mechanisms that may be dissociated from their haemodynamic changes.

Animals↗
PubMed1984

DOCA-salt induced malignant hypertension in spontaneously hypertensive rats.

DOCA-salt hypertension was produced in 10 male 10-week-old normotensive Wistar-Kyoto (WKY) rats receiving deoxycorticosterone acetate (DOCA; 100 mg/kg, subcutaneous pellet) and 1% NaCl drinking water and was compared with data from 10 age- and sex-matched WKY receiving normal tap water (C). These data were also compared with spontaneously hypertensive (SHR) rats similarly treated. After 10 weeks on these programmes, systemic and regional haemodynamics were determined in conscious rats using microsphere techniques. DOCA-salt treatment increased mean arterial pressure (MAP), total peripheral resistance index (TPRI), cardiac and renal weights in both WKY and SHR. In contrast to SHR (C), the SHR (DOCA) demonstrated more severe MAP elevation (204 +/- 4 versus 185 +/- mmHg; P less than 0.01), more severe systemic and regional (especially renal) vasoconstriction, and malignant vasculitis associated with azotaemia and hyperuricaemia. The hyperuricaemia was related inversely to renal blood flow (r = -0.74; P less than 0.01) and directly to renal vasoconstriction (r = 0.65; P less than 0.05) in SHR (DOCA). These data suggest that in both WKY and SHR, DOCA and salt produced marked cardiovascular changes and SHR rats developed malignant hypertension.

Animals↗
PubMed1984

Systemic and regional hemodynamics in normotensive and spontaneously hypertensive rats after slow-channel calcium blocker nitrendipine.

To determine the effects of the recently synthesized slow channel calcium blocker nitrendipine on systemic and regional hemodynamics, mean arterial pressure, heart rate, cardiac index and organ blood flow distribution were measured with the combined radioactive reference sample and microsphere techniques before and one hour after its oral administration (1 mg or 10 mg/kg). Twenty-week-old normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) conscious male rats were studied. At the 10 mg dose, nitrendipine exerted a hypotensive effect within 15 minutes, and this effect persisted throughout the study. After one hour, mean arterial pressure fell by 14 percent of pretreatment levels in WKY controls; it fell by 25 percent in SHR (p less than 0.001). This action was mediated by a fall in total peripheral resistance index (p less than 0.01) that was nonuniformly distributed to the organ circulations since blood flow was maintained or increased to brain, heart, kidneys, lungs, and adrenals, but decreased to skin. No change in cardiac index was observed.

Animals↗
PubMed1984

Nitrendipine: hemodynamic effects in conscious normotensive and spontaneously hypertensive rats.

The effects of immediate (1 h) and prolonged (3 weeks) treatment with nitrendipine on systemic and regional hemodynamics were investigated in Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Mean arterial pressure (MAP) was significantly (p less than 0.05) decreased in both WKY (125 +/- 2 versus 108 +/- 3 mm Hg) and SHR (189 +/- 5 versus 141 +/- 10 mm Hg) 1 h following oral nitrendipine administration (10 mg/kg). This was associated with a significant (p less than 0.05) decrease in total peripheral resistance index (TPRI) (0.48 +/- 0.03 versus 0.38 +/- 0.02 units/kg, WKY; 0.69 +/- 0.04 versus 0.56 +/- 0.05 units/kg SHR) but no change in cardiac index (CI). A significant (p less than 0.05) increase in heart rate (HR) (374 +/- 14 versus 407 +/- 11 beats/min) was observed only in WKY. Vascular resistances were reduced significantly (p less than 0.05) in heart and kidney in both SHR and WKY as well as the brain and splanchnic organs of the WKY. Resistance increased significantly in SHR skin. The MAP reduction with prolonged treatment (196 +/- 3 versus 181 +/- 4 and 150 +/- 5 mm Hg) was also associated with a reduced TPRI (0.73 +/- 0.03 versus 0.64 +/- 0.07 and 0.50 +/- 0.03 units/kg) in SHR treated for 3 weeks with nitrendipine (10 and 20 mg/kg/day, respectively). No changes in systemic hemodynamics were observed in similarly treated WKY. Skeletal muscle and splanchnic vascular resistances were reduced (p less than 0.05) in nitrendipine-treated WKY (20 mg/kg/day).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Hemodynamic studies in spontaneously hypertensive rats with congenital arteriovenous shunts.

Previous studies have demonstrated a subset of normotensive rats (Wistar-Kyoto, WKY) that has arteriovenous shunts and biventricular hypertrophy. In this study, using the combined radioactive reference sample and microsphere techniques, spontaneously hypertensive (SHR) and WKY rats were found to have arteriovenous fistulas, and the magnitude of this shunting was quantified. In both groups with shunts (WKY and SHR, respectively) mean arterial pressure was lower (117 +/- 3 vs. 125 +/- 2 mmHg, NS; 164 +/- 4 vs. 184 +/- 7 mmHg, P less than 0.001) and cardiac index was higher (518 +/- 52 vs. 259 +/- 10 ml.min-1.kg-1, P less than 0.001: 416 +/- 18 vs. 239 +/- 8 ml.min-1.kg-1, P less than 0.001) than in rats without shunts. Both groups demonstrated sizable shunts, with microsphere trapping in 55 +/- 6 and 47 +/- 5% in WKY and SHR, respectively, and reduced blood flow to every organ. These data demonstrate the need for caution in evaluating hemodynamic and myocardial functional data as well as endocrinologic or metabolic functions in WKY and SHR unless shunting is excluded. Moreover, since these subsets seem to have had arteriovenous shunts from birth, it may be inferred that the development of the arterial hypertension in SHR did not result from tissue hyperperfusion.

Animals↗
PubMedDate not supplied

Brain angiotensin and circulatory control.

1. Components of the renin-angiotensin system (RAS) are found in the brain; both outside and inside the blood-brain barrier. 2. Almost all of the classical actions of the brain RAS are attributable to angiotensin (Ang) II and mediated by AT1 receptors. 3. Circumventricular organs (CVO), which lack the blood-brain barrier, are rich in AngII receptors and monitor circulating AngII levels. In vivo binding studies suggest that the CVO are also accessible to cerebrospinal fluid-derived AngII. 4. The median preoptic nucleus, paraventricular hypothalamic nucleus, supraoptic nucleus, nucleus tractus solitarius and ventrolateral medulla are inside the blood-brain barrier and are sites of action of brain AngII. In these nuclei, AngII seems to act as an excitatory neurotransmitter or neuromodulator. 5. Actions of AngII in the brain, both inside and outside the blood-brain barrier, are implicated in the central regulation of blood pressure and sympathetic outflow, release of hypothalamic and pituitary hormones and renal sodium handling. 6. Alterations in the activity of brain AngII may be involved in the mechanisms of some types of hypertension.

Angiotensin II↗
PubMedDate not supplied

Regression of left ventricular hypertrophy in two-kidney, one clip Goldblatt hypertension.

The effect of regression of left ventricular hypertrophy (LVH) on ventricular performance was studied in two-kidney, one clip Goldblatt hypertensive rats (2K1C) treated with methyldopa or by unclipping. Sham operations were performed in a total of 21 rats; 12 and nine were studied after 4 and 6 weeks, respectively. Hypertension was induced in 38 additional rats. Of these, 11 were studied at 4 weeks. Cardiac index was measured by electromagnetic flowmetry under light ether anesthesia, and ventricular performance was assessed by rapid intravenous saline infusion. Of the remaining 27 hypertensive rats at 4 weeks postclipping, 10 were treated with methyldopa (400 mg/kg/day) and nine were unclipped; eight were left untreated as controls. Two weeks thereafter, ventricular performance was determined as described above. When expressed as the relationship between cardiac index and LV end-diastolic pressure, ventricular performance tended to be depressed in 2K1C. Ventricular performance, mean arterial pressure, and LV-to-body weight ratio returned to control in unclipped rats. Whereas methyldopa resulted in regressed LVH, its effect on mean arterial pressure and total peripheral resistance was not as marked as unclipping, both remaining significantly increased (p less than 0.001). The disparate effects of unclipping and methyldopa on systemic hemodynamics indicate that the improved ventricular performance with methyldopa was related more to its effect on LVH, suggesting that in these animals regression of LVH was associated with improved ventricular performance.

Animals↗