CLINICAL AND STEROID METABOLIC STUDIES IN FOUR SIBLINGS WITH CONGENITAL VIRILIZING ADRENAL HYPERPLASIA

1966 ◽  
Vol 52 (4) ◽  
pp. 535-549 ◽  
Author(s):  
Kerstin Hall ◽  
Bernt Hökfelt
Keyword(s):  
Blood Pressure ◽  
Plasma Cortisol ◽  
Salt Intake ◽  
Blood Pressure Response ◽  
Normal Subjects ◽  
Sodium Balance ◽  
Plasma Testosterone ◽  
Plasma Acth ◽  
Adrenogenital Syndrome ◽  
Aldosterone Production

ABSTRACT The present studies were concerned with four siblings suffering from congenital adrenogenital syndrome. Their parents were healthy and not closely related. At first examination the age of the patients varied between 10 and 23 years. They all presented a short stature and marked virilization; blood pressure was normal. All four were genetic females. Three of them were brought up as girls, but one clearly showed male identification. The youngest patient was registered as a boy at birth and brought up as such. None of the case histories revealed signs of cortisol deficiency in spite of low plasma cortisol and low urinary cortisol metabolites. Plasma ACTH was high. Both plasma cortisol and plasma ACTH probably showed normal diurnal variation. Pregnanetriol was a predominant urinary steroid metabolite. There was no indication of a significant secretion of 11-deoxycortisol. Under ordinary salt intake, the urinary aldosterone was higher than in normal subjects, possibly in response to the high production of steroids with natriuretic properties. Following treatment with dexamethasone, the urinary aldosterone decreased and so did cortisol tetra-hydro-derivatives, pregnanetriol and pregnanediol, without any influence on sodium balance. Stimulation with ACTH had no effect on aldosterone production, whereas urinary pregnanetriol and pregnanediol increased markedly, concomitant with a tendency to sodium loss. Angiotensin effectively stimulated aldosterone production, whereas rather larger quantities were needed to obtain a blood pressure response. Plasma testosterone was increased to the levels seen in normal males. Following ACTH there was no further increase in blood testosterone, whereas a marked decrease was seen after dexamethasone. Urinary oestrogens were rather high before treatment and decreased in two patients during treatment with dexamethasone, concomitant with the appearance of urinary gonadotrophins.

VARIATIONS IN PLASMA RENIN ACTIVITY AND URINARY ALDOSTERONE EXCRETION IN NORMAL SUBJECTS AFTER SALT RESTRICTION AND ACUTE PITUITARY INHIBITION WITH 6-DEHYDRO-16-METHYLENE HYDROCORTISONE

1971 ◽  
Vol 67 (1) ◽  
pp. 159-173
Author(s):  
A. Peytremann ◽  
R. Veyrat ◽  
A. F. Muller
Keyword(s):  
Plasma Renin Activity ◽  
Salt Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Inhibitory Effect ◽  
Renin Activity ◽  
Sodium Balance ◽  
Experimental Conditions ◽  
Salt Restriction ◽  
Aldosterone Production

ABSTRACT Variations in plasma renin activity and urinary aldosterone excretion were studied in normal subjects submitted to salt restriction and simultaneous inhibition of ACTH production with a new synthetic steroid, 6-dehydro-16-methylene hydrocortisone (STC 407). At a dose of 10 mg t. i. d. this preparation exerts an inhibitory effect on the pituitary comparable to that of 2 mg of dexamethasone. In subjects maintained on a restricted salt intake, STC 407 does not delay the establishment of an equilibrium in sodium balance. The increases in endogenous aldosterone production and in plasma renin activity are also similar to those seen in the control subjects. A possible mineralocorticoid effect of STC 407 can be excluded. Under identical experimental conditions, the administration of dexamethasone yielded results comparable to those obtained with STC 407.

scholarly journals Effects of AT1A receptor deletion on blood pressure and sodium excretion during altered dietary salt intake

2002 ◽  
Vol 283 (3) ◽  
pp. F447-F453 ◽  
Author(s):  
Amy J. Mangrum ◽  
R. Ariel Gomez ◽  
Victoria F. Norwood
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Wild Type ◽  
Compensatory Mechanisms ◽  
Wide Range ◽  
Blood Pressures ◽  
Pressure Natriuresis

The present study was performed to investigate the role of type 1A ANG II (AT1A) receptors in regulating sodium balance and blood pressure maintenance during chronic dietary sodium variations in AT1A receptor-deficient (−/−) mice. Groups of AT1A (−/−) and wild-type mice were placed on a low (LS)-, normal (NS)-, or high-salt (HS) diet for 3 wk. AT1A(−/−) mice on an LS diet had high urinary volume and low blood pressure despite increased renin and aldosterone levels. On an HS diet, (−/−) mice demonstrated significant diuresis, yet blood pressure increased to levels greater than control littermates. There was no effect of dietary sodium intake on systolic blood pressures in wild-type animals. The pressure-natriuresis relationship in AT1A (−/−) mice demonstrated a shift to the left and a decreased slope compared with wild-type littermates. These studies demonstrate that mice lacking the AT1A receptor have blood pressures sensitive to changes in dietary sodium, marked alterations of the pressure-natriuresis relationship, and compensatory mechanisms capable of maintaining normal sodium balance across a wide range of sodium intakes.

Role of Prostacyclin in Blood Pressure Regulation and Aldosterone Production in Conscious Rabbits

1984 ◽  
Vol 66 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Isamu Miyamori ◽  
Toshio Morise ◽  
Masatoshi Ikeda ◽  
Hideo Koshida ◽  
Yoshiyu Takeda ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Pressure Response ◽  
Control Level ◽  
Ang Ii ◽  
Pressure Regulation ◽  
Aldosterone Production ◽  
Hormonal Action ◽  
Conscious Rabbits

1. The effects of subdepressor infusion of prostacyclin (PGI2, 5.3 pmol min−1 kg−1) on arterial pressure and aldosterone production induced by angiotensin II (ANG II) were studied in conscious rabbits. 2. Indomethacin pretreatment caused an augmented blood pressure response after ANG II infusion, which returned to near control level after concomitant infusion of a subdepressor dose of PGI2. 3. Aldosterone production after ANG II was significantly attenuated after pretreatment with indomethacin. PGI2 infusion restored this reduced response to near control level. 4. These results may suggest that PGI2 in the circulation could also serve to modulate the pressor and hormonal action(s) of ANG II.

scholarly journals A mathematical model of the blood pressure response to salt intake

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Violeta Ivanova Mangourova ◽  
John Ringwood ◽  
Bruce Van Vliet
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Salt Intake ◽  
Blood Pressure Response ◽  
Pressure Response

scholarly journals Histone demethylase LSD1 deficiency and biological sex: impact on blood pressure and aldosterone production

2019 ◽  
Vol 240 (2) ◽  
pp. 111-122 ◽  
Author(s):  
Yuefei Huang ◽  
Pei Yee Ting ◽  
Tham M Yao ◽  
Tsuyoshi Homma ◽  
Danielle Brooks ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Ex Vivo ◽  
Receptor Activation ◽  
Zona Glomerulosa ◽  
Blood Pressure Elevation ◽  
Salt Diet ◽  
Male And Female ◽  
Biological Sex ◽  
Aldosterone Production

Human risk allele carriers of lysine-specific demethylase 1 (LSD1) and LSD1-deficient mice have salt-sensitive hypertension for unclear reasons. We hypothesized that LSD1 deficiency causes dysregulation of aldosterone’s response to salt intake resulting in increased cardiovascular risk factors (blood pressure and microalbumin). Furthermore, we determined the effect of biological sex on these potential abnormalities. To test our hypotheses, LSD1 male and female heterozygote-knockout (LSD1+/−) and WT mice were assigned to two age groups: 18 weeks and 36 weeks. Plasma aldosterone levels and aldosterone production from zona glomerulosa cells studied ex vivo were greater in both male and female LSD1+/− mice consuming a liberal salt diet as compared to WT mice consuming the same diet. However, salt-sensitive blood pressure elevation and increased microalbuminuria were only observed in male LSD1+/− mice. These data suggest that LSD1 interacts with aldosterone’s secretory response to salt intake. Lack of LSD1 causes inappropriate aldosterone production on a liberal salt diet; males appear to be more sensitive to this aldosterone increase as males, but not females, develop salt sensitivity of blood pressure and increased microalbuminuria. The mechanism responsible for the cardiovascular protective effect in females is uncertain but may be related to estrogen modulating the effect of mineralocorticoid receptor activation.

Cardiovascular Responses to Sustained Handgrip in Normal Subjects and in Patients with Diabetes Mellitus: A Test of Autonomic Function

1974 ◽  
Vol 46 (3) ◽  
pp. 295-306 ◽  
Author(s):  
D. J. Ewing ◽  
J. B. Irving ◽  
F. Kerr ◽  
J. A. W. Wildsmith ◽  
B. F. Clarke
Keyword(s):  
Diabetes Mellitus ◽  
Blood Pressure ◽  
Blood Pressure Response ◽  
Muscle Tension ◽  
Maximum Voluntary Contraction ◽  
Pressure Rise ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Simple Method ◽  
Patients With Diabetes

1. The blood pressure and heart rate responses to static muscular exercise were measured in sixty normal subjects and 124 patients with diabetes mellitus, aged 25–54 years, during a standardized sustained handgrip test at 30% maximum voluntary contraction (MVC). 2. The normal range of the response was established. Females had a smaller blood pressure rise than males, and their MVC was lower. In the normal subjects there was a significant correlation between the size of the MVC and the height of the blood pressure response. The absolute muscle tension exerted should be taken into account in addition to the percentage MVC, when comparing responses to sustained exercise in different disease states. 3. The diabetic subjects showed a similar sex difference in their response. The mean diastolic blood pressure rises were smaller than in the control groups, both in males and females, but this was related to a smaller mean MVC. 4. Twenty-two of the diabetic subjects had an abnormally low response to sustained handgrip, which was not related to age, duration of diabetes, treatment or control of the disease. These diabetic subjects probably had damage of the autonomic fibres mediating the response. The findings would suggest that sustained handgrip is a useful and simple method of detecting involvement of the autonomic nervous system in diabetes.

Effect of age and gender on sudomotor and cardiovagal function and blood pressure response to tilt in normal subjects

1997 ◽  
Vol 20 (12) ◽  
pp. 1561-1568 ◽  
Author(s):  
Phillip A. Low ◽  
Jong-Chyou Denq ◽  
Tonette L. Opfer-Gehrking ◽  
Peter J. Dyck ◽  
Peter C. O'Brien ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Normal Subjects ◽  
Pressure Response ◽  
Age And Gender ◽  
And Gender ◽  
Effect Of Age

Interactions between subtotal nephrectomy and salt: effects on blood pressure and renal function in pregnant and nonpregnant ewes

2008 ◽  
Vol 294 (4) ◽  
pp. R1227-R1233 ◽  
Author(s):  
Karen J. Gibson ◽  
Amanda C. Boyce ◽  
Clare L. Thomson ◽  
Sarah Chinchen ◽  
Eugenie R. Lumbers
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Salt Intake ◽  
High Salt ◽  
Late Gestation ◽  
Plasma Creatinine ◽  
Sodium Balance ◽  
Sodium Reabsorption ◽  
High Salt Intake ◽  
In Pregnancy

The effects of high salt intake on blood pressure and renal function were studied in nine subtotally nephrectomized pregnant ewes (STNxP) and seven intact pregnant ewes (IntP) in late gestation and in eight subtotally nephrectomized nonpregnant ewes (STNxNP) and seven intact nonpregnant ewes (IntNP). STNxP had higher mean arterial pressures ( P < 0.02) and plasma creatinine levels ( P < 0.001) than IntP. High salt (0.17 M NaCl as drinking water for 5 days) did not change blood pressure in either STNxP or IntP. STNxNP had higher mean arterial pressures ( P = 0.03) and plasma creatinine levels ( P < 0.001) than IntNP. In STNxNP, blood pressure increased with high salt intake and there was a positive relationship between diastolic pressure and sodium balance ( r = 0.497, P = 0.05). This relationship was not present in IntNP, STNxP, or IntP. Because high salt intake did not cause an increase in blood pressure in STNxP, it is concluded that they were protected by pregnancy from further rises in blood pressure. The observed increase in glomerular filtration rate ( P < 0.03) and depression of fractional proximal sodium reabsorption ( P = 0.003) that occurred in STNxP, but not in STNxNP, in response to high salt may have contributed to this protection. As well, the increased production of vasorelaxants in pregnancy may selectively protect against the occurrence of salt-sensitive hypertension in pregnancy.

scholarly journals Salt intake and blood pressure response to percutaneous renal denervation in resistant hypertension

2017 ◽  
Vol 19 (11) ◽  
pp. 1125-1133 ◽  
Author(s):  
Esther de Beus ◽  
Rosa L. de Jager ◽  
Martine M. Beeftink ◽  
Margreet F. Sanders ◽  
Wilko Spiering ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Resistant Hypertension ◽  
Renal Denervation ◽  
Salt Intake ◽  
Blood Pressure Response ◽  
Pressure Response
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