ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY The interrelationship of blood pressure, cardiac output, and peripheral resistance was studied in Dahl "S" and "R" rats after 3 days on a high (8%) NaCl diet. Both "S" and "R" rats were nonnotensive when fed a normal (0.3%) NaCl diet. After 3 days of the high NaCl diet, the "R" rats remained normotensiTe (BP 112 mm Hg), while the "S" rats had an elevation of arterial pressure (BP 133 mm Hg) (p< 0.001). The cardiac outputs of both "S" and "R" rats were similar on the low NaCl diet. After 3 days high NaCl feeding, the cardiac output of the "R" rats rose 18% above "R" control level (p< 0.0001), while the peripheral resistance declined 14% below the "R" control level (p< 0.005), and the blood pressure (BP) did not change, a pattern quite contrary to the concept of "whole-body" autoregulation. With a similar 3-day high NaCl feeding in "S" rats, cardiac output (p< 0.005) and peripheral resistance (p< 0.05) both increased 10%, while BP rose 20%. After 7 days of high NaCl feeding, the cardiac output of the "S" rats had returned to normal, while blood pressure and peripheral resistance both continued to be elevated. This pattern of response in "S" rats could be compatible with the concept of "whole-body" autoregulation. However, since both NaCl hypertension and Goldblatt hypertension can occur in settings in which "whole-body" autoregulation appears not be to causally related, one cannot be certain whether "whole-body" autoregulation is playing a causal role in the mechanism of NaCl-induced hypertension in "S" rats. It is a striking dichotomy that 3 days of high salt feeding produces vasoconstriction in "S" rats and vasodilation "R" rats.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Two-kidney, one clip Goldblatt rats were treated with oral converting enzyme inhibitor captopril (SQ 14,225) 6 mg/kg/day for 3 weeks after they had developed hypertension. Before treatment, systolic blood pressure rose from 143 to 202 mm Hg (p< 0.05). Tail vein infusions of saralasin 10 $ig/kg/min in conscious rats reduced systolic blood pressure from 202 to 121 mm Hg (p< 0.05) at 8 weeks after clipping the renal artery and before treatment with captopril. Chronic treatment with captopril for 3 additional weeks lowered blood pressure to 173 mm Hg (p< 0.05). When saralasin infusion was repeated during treatment with captopril, blood pressure fell from 173 to 159 mm Hg (p< 0.05). Blood pressure rose to 197 mm Hg within 4 days after captopril was discontinued and saralasin infusion 3 weeks after captopril (15 weeks after clipping the renal artery) again resulted in a dramatic fall in blood pressure from 197 to 142 mm Hg (p< 0.05). Goldblatt rats who had not received captopril showed no blood pressure response to saralasin infusion at 12 weeks after renal artery clipping. The present study demonstrates that partial inhibition of the reninangiotensin system with captopril results in a delay in the natural evolution of clip hypertension retarding the appearance of hypertension that is resistant to acute saralasin infusion.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY The mechanism by which the angiotensin I (AI) converting enzyme inhibitor SQ20,881 (<Glu- Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro) blocks the pressor response to exogenous AI was studied in mo in the intact anesthetized dog. When administered as a single dose 250 times that of Injected AI (250 nmoles/kg) into either the pulmonary or systemic circulation, SQ20,881 produced inhibition of pulmonary conversion of exogenous AI to AH that lasted for more than 6 hours as judged by the absence of immunoreactive or labeled AH in the pulmonary venous effluent. In contrast, the pressor response to exogenous AI began to reappear within 1 hour of SQ20.881 administration. Six hours following SQ20.881, the pressor response to AI had nearly returned to normal, still in the absence of demonstrable intrapulmonary conversion and without release of detectable amounts of All into the pulmonary venous effluent. These experiments demonstrated that AI has a pressor effect in the presence of SQ20.881 that is independent of pulmonary conversion. Studies with (Des- Asp1) AH and (Des-Asp, Arg") AH snowed that the delayed pressor response to AI following SQ20.881 administration could not be accounted for by circulating peptide metabolites of AI or AH. A competitive inhibitor of AH, (D-Asp 1, lie*) AH completely blocked the returning pressor response, suggesting that extrapulmonary generation of AH was responsible. The data strongly suggest that the systemic vascular bed taken as a whole contains large amounts of AI converting enzyme that is capable of rapid generation of AH without releasing the peptide into circulation. The extrapulmonary enzyme is more resistant to long-lasting blockade by SQ20,881 than pulmonary converting enzyme. The physiological role of extrapulmonary conversion in systemic and local circulatory homeostasis remains to be assessed.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY The bemodynamic response to mental stress (mental arithmetic) was studied in adolescents with varying risk factors for essential hypertension (EH). One group (genetic) consisted of nonnotensive well adolescents who had at least one parent with EH. Another group (labile) consisted of adolescents with labile hypertension each of whom also had at least one parent with EH. The control population consisted of normotensive adolescents with a negative family history of EH. Subjects with labile hypertension demonstrated a sustained increase in systolic and diastolic pressure and heart rate during stress. This response was significantly different than the control population (p< 0.001). The stress response of the nonnotensive genetic population was qualitatively similar to the group with labile hypertension and significantly different than the controls in diastolic pressure and heart rate (p< 0.001, < 0.02). Post-stress plasma catecholamines were higher in the labile hypertensive and genetic groups than in the control group. These findings demonstrate increased central nervous system mediated adrenergic activity and cardiovascular response in labile hypertension and also in some normotensive subjects with a genetic risk for hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Experiments were performed to determine the role of vasopressin in deoxycorticosterone (DOC)-salt hypertension. In order to determine if vasopressin is necessary for the development of DOC-salt hypertension, rats with hereditary diabetes insipidus (DI) and normal Long-Evans rats (LE) were unilaterally nephrectomized, treated with DOC Pivalate (30 mg/kg week) and given saline to drink for 8 weeks. A second group of DI rats were unilaterally nephrectomized, but received no treatment. Systolic blood pressure (SBP) increased 40 mm Hg in the LE group (p< 0.01) but failed to increase significantly in either DI group. Urinary excretion of vasopressin (UADHV) and SBP were measured in unilaterally nephrectomized LE rats treated with DOC and salt (DOC-LE), salt alone (NaCI-LE) and untreated rats (H.O-LE). The UADHV was elevated in DOC-LE (j> < 0.01) and NaCI-LE (p< 0.05) rats, but only the DOC-LE rats became hypertensive. Finally, the I.V. injection of analogs of vasopressin, which block its pressor but not antidluretic activity, lowered mean arterial blood pressure 27 ± 5 mm Hg in 11 conscious DOC-salt hypertensive rats. It is concluded that vasopressin plays a major role as a pressor agent in both the onset and maintenance of DOC-salt hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY The short-terra cardiovascular and endocrine effects of an orally active anglotensin converting enzyme inhibitor, SQ14,225, were evaluated in 17 subjects with drug-resistant hypertension (10 with essential and seven with renovascular hypertension). On normal dietary sodium, SQ 14,225 (after 3 days at average doses of 664 mg/day) reduced mean arterial pressure (MAP) significantly (from 141 ± 4 to 122 ± 4 mm Hg, (SE), p< 0.001). However, only eight of the patients achieved blood pressures within the normotensive range.Of eight patients with residual hypertension, seven exhibited further decreases in MAP (from 132 ± 4 to 108 ± 6 mm Hg (SE),p< 0.001) when dietary sodium was reduced to 10 mEq/day. No rebound hypertension was noted when treatment was temporarily discontinued for 3 days in 11 patients. The reductions in blood pressure were not associated with either orthostatic hypotension or interference with baroreceptor reflexes.The values of supine plasma rerun activity (PRA) were not always predictive of blood pressure responsiveness to the drug. With treatment, plasma aldosterone concentrations (PAC) decreased modestly (values from 40 ± 9 to 22 ± 3 ng/dl (SE),p< 0.05). The plasma concentrations of cortisol, norepinephrine and serum potassium were left unchanged during the period of studies.The present study has not defined the exact mechanism by which SQ 14,225 lowered blood pressure. Nevertheless, it indicates that this agent may be a practical therapeutic adjunct in the treatment of certain subsets of the human hypertensive population. The lack of serious interference with cardiovascular and humoral homeostasis adds to its attractiveness as a therapeutic agent.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY The activity of serum dopamine-hydroxylase (DBH) was measured in 1194 asymptomatic middle-aged men with diastolic blood pressure ranging from 75 to 125 mm Hg during the baseline examination of a multifactorial intervention program for primary prevention of coronary heart disease. No correlation was present between serum DBH activity and systolic (r= − 0.01, NS) or diastolic (r= + 0.02, NS) blood pressure. No significant differences in serum DBH actirity was observed between individuals with blood pressure in the lower, middle or upper deciles. Serum DBH activity was similar in subjects with normal blood pressure, in individuals with widely fluctuating blood pressure and patients with fixed hypertension. The results suggest that serum DBH activity cannot be used as an aid in the diagnosis of essential hypertension of middle-aged men.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY A renin-like enzyme and add protease (cathepsin) from whole and saline-perfused dog brains were separated by CM-cellnlose cbromatography with a linear NaCl gradient. Plasma renin and cathepsin were also separated using the same system. During the separation steps (in all the above cases) the specific activity of the brain renin-like enzyme was increased, while the specific activity of the brain cathepsin was decreased. Approximately a 70-fold increase in the specific activity of brain renln-like enzyme and a sixfold decrease in brain cathepsin specific activity was obtained from saline-perfused brain. The separation made it possible to study the pH optimum of the brain renin-like enzyme and acid protease. The brain renin-like enzyme showed optimal activity in the range of pH 6-7. Immunologically, the renin-like enzyme was distinctly different from dog kidney renin.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID