ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Rabbit brain endo-oligopeptidase B inactivates angiotensin I (Asp-Arg-Val-Tyr-Ile-His-Pro- Phe-His-Leu) and angiotensin II (Asp-Arg-Val-Tyr-Ile-Hls-Pro-Phe) by hydrolysis of the Pro'-Phe4peptide bond. The site of hydrolysis was determined in preparative and analytical experiments in which both products were recovered in a molar ratio of 1:1, and the sum of the products plus unhydrolyzed substrate accounted for the starting material. The enzyme has a Km of 6.3 × 10−5M for angiotensin II at pH 8.3 and is activated 30- fold with 4.8 mM dlthlothreitol. BPP90(<Gui-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro, SQ 20,881) inhibits the Inactivation of angiotensin II with an I50of 5 × 10−5M. BPP64(<Glu-Lys-Trp-Ala-Pro, SQ 20,475) is less active and D-3-mercapto-2-methylpropanoyl-L-proline (captopril, SQ 14,225) has essentially no activity. These compounds are significantly more potent as inhibitors of angiotensln-converting enzyme. The role of brain endo-oligopeptidase B in angiotensin I and II metabolism remains to be established. (Hypertension 4: 178–184, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The role of angiotensinogen ID blood pressure control was assessed in nonnotensive rate by observing the changes resulting from inhibition by specific rat angiotensinogen antiserum. The antiserura decreased blood pressure in rats on normal sodium as well as sodium-free diets (respectively ΔBP = −30 ± 6 mm Hg and −42 ± 8 mm Hg). In binephrectomlzed sodium-replete rats, administration of antiserum did not reduce blood pressure, whereas in sodium-depleted animals it slightly decreased blood pressure by 11 ± 3 mm Hg. These results suggest that angiotensinogen participates in the regulation of blood pressure in normotensive rats, even in the sodium-replete state. (Hypertension 4: 185–189, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Twenty-three patients with different degrees of renal insufficiency were studied after equilibration on two levels of salt intake. Blood pressure was found to increase after increased salt intake. This blood pressure increase, when related to sodium excretion increase (salt sensttirity index), tended to be larger in patients with a greater loss of kidney function. In fact, the salt sensitivity of blood pressure rose exponentially with tbe decline of the kidney function, which resulted In a linear negative relationship between tbe log of salt sensitivity index and creatinine clearance (r − 0.89,p< 0.0001). After increased salt intake, plasma renin activity (PRA) decreased, whereas body-fluid volumes Increased. Concotnitantly, the products of log PRA and extracellular-fluid volume or blood volume decreased (p< 0.005). Weak interrelations were found between increases of body fluid volumes and blood pressure (r − 0.49,p< 0.05). When the patients were divided into two groups according to creatinine clearance, Group 2 (creatinlne clearance < 22 ml/mln,n= 13) showed a significantly greater increase of blood pressure for any given expansion of extracellular fluid volume than Group 1 (creatinine clearance > 32 ml/mln, n − 9). Moreover, for any given increase in sodium excretion blood volume increased more in Group 2 than in Group 1 (p< 0.03), whereas the increase of extracellular fluid volume was similar in the two groups. Consequently, after increase of salt intake the plasma volume/interstitial fluid volume ratio (PV/IF) tended to decrease in Group 1 and to increase in Group 2. This difference In PV/IF ratio behavior was significant (p< 0.01). A significant interrelation was also found between the salt sensitivity index and change of PV/IF ratio (r = 0.60,p< 0.01). It is concluded that, with decrease in functioning renal mass, the salt sensitivity of tbe blood pressure increases. This increase in salt sensitivity is accompanied by an increased intra/extravascular-fluld volume ratio after salt loading, which suggests a change of tissue-capillary filtration forces in patients with renal insufficiency. (Hypertension 4: 190–197, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

One-kidney, one clip hypertension may be caused by a renal humoral factor that is not renln. In the search for such a factor, Skeggs and coworkers have provided evidence that certain extracts of rabbit kidneys can increase the blood pressure of other rabbits Indefinitely by a mechanism having a slow onset. In the present experiments an ethanol extract of rabbit kidneys and an acetone extract of a 2.0–4.0 M ammonium sulfate precipitate were injected into rabbits for 10 to 12 days. By Day 3 the Increase in blood pressure (mm Hg) was only 1 ± 3 and 7 ± 2, respectively, but by the end of the injection period, blood pressure had increased by 21 ± 4 (p< 0.025) and 19 ± 4 {p< 0.005). Several weeks later the blood pressure was still significantly elevated above control: 13 ± 2 (p< 0.005) and 15 ± 5 (p< 0.05). A similar pattern of response was seen in unilaterally nephrectomized rabbits. In contrast, injection of an ethanol extract of rat kidneys or a 0.75–2.0 M ammonium sulfate fraction or a 2.0–4.0 M ammonium sulfate fraction or an acetone extract of the latter had no effect on the blood pressure of rats when injected at comparable doses for 13 to 15 days. The ethanol extract of rabbit kidneys caused a mild increase in the blood pressure of rats, but this was not significant. No increase in blood pressure was seen when renal cells from rats with one-kidney, one clip hypertension were Injected lutraperitoneally into normal rats. Therefore, although the present experiments support the existence of renopressin in rabbit kidneys, a similar factor could not be demonstrated in extracts of rat kidneys. (Hypertension 4: 198–204, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Erythrocyte sodium efflux as well as sodium, potassium, and water content were studied in 12 untreated men with uncomplicated essential hypertension and in 18 normotensive control subjects. In the patients with essential hypertension, the rate constant for total sodium efflux was significantly lower than in the nonnotensives (5.96-10−2± 0.45–10−3min−1vs 6.69.10−2' ± 0.49-10−1'> < 0.005), which was due to a reduced ouabain-sensitire sodium efflux rate constant. Significant differences in total sodium efflux and ouabaln-sensitire sodium efflux, however, could not be demonstrated, since intracellular sodium concentrations, although insignificant, were higher in the patients with essential hypertension (6.11 ± 0.74 mmole/Hter vs 5.97 ± 0.66 mmole/llter. The rate constants for ouabain-lnsensltiTe sodium efflux, for ouabaln-lnsensitive furosemide-sensitire sodium efflux, and for passive (ouabain-insensitive furosemlde-insensitive) sodium efflux were similar in hypertensives and in normotenslves.The cause of the reduced rate constant for ouabaln-sensltive sodium efflux is not clear. However, as suggested for other types of altered erythrocyte transport mechanisms described recently, it might be determined genetically. (Hypertension 4: 205–210, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

We isolated renin granules from cadaver kidneys using discontinuous sucrose density gradient centrifugation, and investigated the storage form of the renin from these granules. Approximately 23% of the total renin activity in the original bomogenate was obtained from the surface phase between 1.6 and 1.7 M sucrose (Fraction 6). Granule renin extracted from the granules in Fraction 6 was separated into active and inactive renin using pepstatin affinity chromatography. Only the active renin had an affinity for pepstatin. The inactive renin, albeit activated by trypsln, was little activated by acidification. The proportion of inactive renin was about 25% of the total granule renin (active renin + inactive renin). Trypsln concentrations over 10 μg/m resulted in a decrease in the renin activity of the trypsln-activated renin, but the enzymatic activity of active renin was decreased by trypsln. With gel filtration, the Inactive renin revealed a single peak, and the molecular weight (MW)was 48,000. The active renin had a MW of 44,000. The inactive renin could be activated by trypsln without an apparent change in molecular weight. (Hypertension 4: 211–218, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The present study assessed the contribution of the renin-angiotensln system (RAS), dietary sodium, and cardiac output (CO) to the genesis of primate hypertension in a one-kidney model which was developed to test species-specific renin inhibitors. Reduction of renal perfusion pressure increased mean arterial pressure (MAP) from 105 ± 4 to 127 ± 3 mm Hg (p< 0.0005), associated with increased plasma renin activity (PRA) from 4.9 ± 0.7 to 13.8 db 1.1 ng.ml−1hr−1(p< 0.0005). Correlation of MAP with PRA yielded an r value of 0.662 (p< 0.0005). Significant blood pressure elevation was obtained with both regular (R) and low sodium (LS) diet (p< 0.0005), although the MAP change was greater with LS. With both R and LS diet, hypertension was associated with increased PRA (p< 0.0005), and normotensive pressures were achieved with converting enzyme inhibitor (teprodde). The hemodynamic change with hypertension was an increase of systemic vascular resistance (SVR) from 0.89 ± 0.12 to 1.17 ± 0.09 units {p< 0.05); cardiac output (CO) and central blood volume did not change significantly. Thus, acute hypertension, mediated by the RAS, was developed in a one-kidney primate model. The hemodynamic correlate of hypertension was increased SVR; CO and volume redistribution were not Initiating factors. (Hypertension 4: 219–225, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

In IS normotensive subjects, 17 newly diagnosed, untreated hypertensive patients, and 22 effectively treated hypertensive patients, a battery of neuropsychological tests was given. All subjects were neurologically asymptomatic. The neuropsychological battery included tests evaluating global cognitive functions (Card Sorting Test, Wechsler Memory Scale, Progressive Matrices 1938), as well as specific cognitive functions (Benton Test, subtests of the Wechsler-Bellevue Scale). Normotensive controls obtained better scores in all the tests. Statistical analysis of the scores suggests that hypertension is highly correlated with impairment of memory, logical reasoning, visuospatial organization, and attention. Therapy seems to impair attention, while the duration of disease seems to influence visuospatial performances. (Hypertension 4: 226–229, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Aldosterone is known to stimulate Na+transport as measured in terms of current-carrying capacity of epithelial sheets or of Na+— K+ATPase activity in cells. The possibility that this is reflected in an altered steady-state transmembrane Na+distribution in vascular smooth muscle was here examined directly. Transmembrane Na+and K+gradients were first dissipated by orernlght incubation in K-free physiological salt solution (PSS) at 10°C and then reesUblished by 3 hours in normal PSS at 37°C. The addition of d-aldosterone (but not corticosterone) to these media significantly reduced cell Na. This involved only free cell Na which was reduced by about 20% or 3 mmole/kg dry wt. No significant change in membrane permeability measured in terms of net Li uptake at 3°C or at 37°C was observed. The lowest effective aldosterone concentration was 2.8 × 10−2M. These results are consistent with the observed enhancement of net Na+transport in incubated arteries in DOCA-induced hypertension and in the SHR but do not account for the increased Na+permeability observed in these states. (Hypertension 4: 230–237, 1982)

ISSN:0194-911X    

出版商:OVID    

年代:1982

数据来源: OVID