Nocturnal Blood Pressure and Relation to Vasoactive Hormones and Renal Function in Hypertension and Chronic Renal Failure

Abstract

The purpose of this study was to assess the blood pressure profile and to measure vasoactive hormones in patients with essential hypertension (n=61), secondary hypertension (n=32) and chronic renal failure (n=32) matched with healthy control subjects (n=35), and to study the relationship between circadian changes in blood pressure and baseline levels of vasoactive hormones and renal function. Non-invasive, automatic blood pressure measurement was performed for 24 or 48 h. Venous plasma concentrations of renin, angiotensin II, aldosterone, arginine vasopressin, atrial natriuretic peptide and endothelin were measured. The mean 24-h blood pressure was higher in all groups of hypertensive patients than in control subjects. The nocturnal blood pressure fall was preserved in essential hypertension, in contrast to secondary hypertension in which it was attenuated. In the patients with chronic renal failure the 24-h mean blood pressure was the same as in the controls. Night-time blood pressure was higher among the chronic renal failure patients than in the control group, and the nightly blood pressure fall in both diastolic and systolic blood pressure was reduced. Plasma concentrations of renin activity, arginine vasopressin, atrial natriuretic peptide, aldosterone and endothelin were significantly increased in secondary hypertension and chronic renal failure, compared to essential hypertension and control subjects. Plasma angiotensin II was increased in chronic renal failure compared to essential hypertension and controls. Estimated creatinine clearance and nightly blood pressure dips were inversely correlated in essential and secondary hypertension, i.e. with a decreasing renal function both systolic and diastolic nightly blood pressure dips were gradually attenuated. In the whole group of patients the nightly systolic and diastolic blood pressure dips were negatively correlated to basal plasma renin activity, plasma aldosterone and atrial natriuretic peptide levels, i.e. the higher the basal plasma hormone level the lower the blood pressure dip. In conclusion, patients with essential hypertension have elevated but normally configured 24-h blood pressure profiles, and patients with different kinds of secondary hypertension have elevated 24-h blood pressure profiles and attenuated nightly systolic and diastolic blood pressure falls. The more the renal function is reduced and the more the plasma levels of renin and aldosterone are increased, the more the nocturnal fall in blood pressure is reduced. It is suggested that the attenuated or absent decrease in nocturnal blood pressure in secondary renal hypertension is caused by an abnormally increased secretion of vasoactive hormones and/or by so far unknown factors released from the diseased kidney.

AT 1 Receptor Blockade Improves Vasorelaxation in Experimental Renal Failure

“…25 The synthesis of these peptides is upregulated in pressure and volume overload, 20,[25][26][27] as in patients with renal failure. 28,29 In this study, the ventricular levels of ANP mRNA were increased in NTX groups, whereas elevated levels of NT-proANP in plasma indicate that the release of ANP was increased. 25 Ventricular concentrations of BNP mRNA and BNP peptide were also increased in NTX rats.…”

Blood pressure and progression of chronic kidney disease: Importance of systolic, diastolic, or diurnal variation

“…In a study of normotensive (n = 27) and hypertensive (n = 41) patients with chronic renal insufficiency, and matched control groups, the renal patients showed significantly blunted nocturnal pressure reduction compared with their respective control groups (P < 0.01 and P < 0.001, respectively), wider distribution of BP values; and a greater nocturnal variability [38]. Similarly, Jensen and Pedersen [39] studied patients with essential hypertension (n = 61), secondary hypertension (n = 32), and chronic renal failure (n = 32) matched with healthy control subjects (n = 35), and demonstrated that nighttime BP was higher among the chronic renal failure patients than in the control group, and the nightly fall in BP was reduced. Similar data about the lack of nocturnal BP decline in patients with chronic renal insufficiency have been reported in other studies [40,41].…”

Disturbed Circadian Rhythm of Urinary Albumin Excretion in Non-Dipper Type of Essential Hypertension

“…In addition, we found [14] that the GFR was an independent factor affecting the nocturnal MAP fall in the sodium-sensitive type of essential hypertension. A positive correlation between GFR and nocturnal BP dip was also reported in both essential hypertension and chronic renal failure [23]. These findings suggest that the circadian rhythm of the BP is determined at least in part by the kidneys and their sodium handling.…”