Research Area

Blood Pressure Regulation


Normal blood pressure rhythm changes

Under normal physiological conditions, the fluctuation of human blood pressure is characterized by a near-day rhythm (or circadian rhythm). As body position changes, exercise, and digests food, blood pressure levels are constantly changing, even when sleeping at night. Blood pressure generally peaks after resumes activity in the morning, and then falls to a trough at 2 to 5 before dawn. During sleep, blood pressure is 10-20 mmHg (1 mmHg-0.1333 kPa) lower. Under normal circumstances, when the human body is changed from a lying position to a standing position, the systolic blood pressure can be slightly lowered (<10 mmHg) and diastolic blood pressure can be slightly increased (about 2.5 mmHg).

Blood Pressure Regulation

Factors related to the regulation of blood pressure rhythm

Arginine vasopressin (AVP)

Arginine vasopressin (AVP) is a hormone synthesized as a peptide prohormone in neurons in the hypothalamus, and its secretion is regulated differently from peripheral AVP. Kellner et al found that AVP can enhance corticotropin-releasing hormone activation of the thalamus-pituitary-adrenal system, enhance the early and late secretion of ACTH and enhance the secretion of corticosteroids at night.

Renin-angiotensin-aldosterone system (RAAS)

RAAS is an important system for regulating blood pressure rhythm. Phoon et al. randomly use placebo or angiotensin-converting enzyme (ACE) inhibitor (captopril) to treat six volunteers, and found that the latter's blood pressure was significantly lower than the former, indicating that angiotensin is a factor in blood pressure regulation. Stepien et al found that there was a 24h rhythm change in ACE in normal blood pressure mouse (WKY) serum, whereas in high blood serum, ACE activity did not change with time. In transgenic hypertensive rats, Schnecko et al. injected an angiotensin II receptor inhibitor (losartan) and an ACE inhibitor (enalapril), respectively, and found that blood pressure decreased, and the originally reversed blood pressure rhythm was corrected. This indicates that RAAS is one of the important mechanisms that cause changes in hypertension and blood pressure rhythm.

Atrial natriuretic peptide (ANP)

ANP is another important substance regulating blood pressure rhythm, mainly through three aspects: (1) regulating renal function and blood vessel force; (2) opposite to RAAS; (3) functioning in the central blood pressure regulation zone. Eventually reduce blood volume and blood pressure. However, if blood volume or blood pressure changes cause life-threatening, the effect is quickly offset. In patients with hypertensive renal failure and hypotensive heart failure, nocturnal blood pressure is not reduced, and the corresponding ANP is not the peak of secretion at night. In hemodialysis patients, the blood pressure rhythm changes, and the corresponding ANP also changes, showing an increase in ANP before and after dialysis. Sothem et al. found that ANP has significant rhythmic changes in studying the relationship between ANP and blood pressure rhythm. At the highest peak of 4 am, the concentration was 2 times higher than that in the afternoon and evening, and the blood pressure value was significantly negatively correlated with the value of ANP (P<0.001). It is indicated that ANP plays an important role in the maintenance of blood pressure and the regulation of rhythm.

Calcitonin gene-related peptide (CGRP)

CGRP is a 37 amino acid polypeptide with potent vasodilator effects. In primary hypertensive rats, CGRP level is declining. At the center, injecting CGRP into the amygdala (which is the cardiovascular regulatory center) can cause an increase in blood pressure. In the periphery, the function of vasodilation of CGRP can be achieved by: (1) activating the K-ATP channel on smooth muscle; (2) mediated by a second messenger cAMP, and then still partially passing through the K-ATP channel; (3) mediating changes in intracellular calcium; (4) mediates vasoconstrictor decline through progesterone.

Sympathetic adrenal medulla system

The sympathetic adrenal medulla system has a strong vasoconstriction effect, but does not play a major role in the regulation of blood pressure rhythm. In the experiment of Phoon et al., dexamethasone and ampoules were used in 6 volunteers respectively, and no change in blood pressure rhythm was found.

Central regulation of blood pressure rhythm

Stoynev et al. believes that the anterior hypothalamus (AH) is the central regulator of blood pressure regulation. The suprachiasmatic nucleus (SCN) in AH is an important region in the regulation of blood pressure rhythm. In the experiment, AH tissue of the primary hypertensive mouse embryo was transplanted into the normal blood pressure mouse, and the latter blood pressure rhythm disappeared. After destroying the SCN of transgenic mice and normal mice, the blood pressure rhythm disappeared. Jin et al. found that one cell in the SCN stayed active at 24h rhythm, which can correct the defects of the body clock and improve the circadian rhythm of the body. At least six proteins were found in the SCN to precisely control other genes to "open" and "close" with the 24 rhythm. One of the regular release of the AVP gene in specific regions of the brain is controlled by a protein produced by the central clock gene.

Relationship between disease and blood pressure regulation

In clinical studies, it was found that the fluctuation of blood pressure in essential hypertension was similar to that of normal people. However, due to the morphological changes of blood vessel wall and progressive cardiac dysfunction in hypertensive patients, the blood pressure at night was not significantly decreased, and the blood pressure stability during waking was poor. The circadian rhythm of patients with secondary hypertension is opposite to that of normal people. In patients with cerebral infarction, blood pressure does not decrease at night, and it rises. This is related to the infarction site. Infarction in the insula and cortex is significantly associated with changes in blood pressure rhythm. The infarction in the right cerebral hemisphere has a greater effect on blood pressure rhythm than in the left cerebral hemisphere. The changes in blood pressure rhythm caused by brain stem infarction are larger than cortical infarction. In the study of patients with schizophrenia, blood pressure change of chronic patients with remission or no medication is the same as normal. In the medication treatment period, the blood pressure rhythm is changed. Explain that these drugs can affect blood pressure rhythm changes. Through the above research, our understanding of the regulation of blood pressure has been further deepened. This provides us with new ideas for the diagnosis and treatment of cardiovascular diseases.

References:

  1. Soergel M, et al. Oscillometric twenty-four-hour ambulatory blood pressure values in healthy children and adolescents: a multicenter trial including 1141 subjects. J Pediart. 1997, 130(2): 178-184.
  2. Mazur ES, et al. Clinical significance of blood pressure variability in hypertension. Ter Arkh. 1999, 71(1): 22-25.
  3. Ruschitzka F, et al. Longitudinal study of 24-hour blood pressure behavior in pregnancy and puerperium in patients with normal pregnancy, pre-eclampsia and HELLP syndrome. Z Geburtshilfe Neonatol. 1996, 200(3): 100-103.
  4. Dawson SL, et al. Diurnal blood pressure change varies with stroke subtype in the acute phase. Stroke. 1998, 29(8): 1519-1524.
  5. Fukudome Y, et al. Circadian blood pressure in patients in a persistent vegetative state. Am J Physiol. 1996, 270 (5 Pt 2):R1109-1114.
  6. Phoon RK, et al. The role of the hypothalamic-pituitary-adrenal (HPA) axis in the regulation of blood pressure. Clin Exp Hypertens. 1997, 19(4): 417-430.
  7. Schnecko A, et al. Effects of the angiotensin II receptor antagonist losartan on 24-hour blood pressure profiles of primary and secondary hypertensive rats. J Cardiovasc Pharmacol. 1995, 26(2): 214-221.
  8. Stoynev AG, et al. Suprachiasmatic nuclei lesions eliminate the group circadian rhythm of systolic arterial pressure but not of heart rate in rats. Acta Physiol Pharmacol Bulg. 1996, 22(1): 1-6.

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