The relationship of stress and blood pressure effectors

Abstract

Exaggerated cardiovascular response to acute and chronic stresses increases the risk for hypertension and cardiovascular disease. Stress also can be broadly defined as a disruption of homeostasis. The re-establishment and maintenance of homeostasis entail the coordinated activation and control of neuroendocrine and autonomic stress systems. Stressor-related information from all major sensory systems is conveyed to the brain. Brain activates neural and neuroendocrine systems to minimize the harmful effects of stress. Stress is generally thought to contribute to the development of hypertension. On the other hand, the evidence is still inconclusive. It is generally accepted that stress-induced hypertension occurs because of increases in sympathoadrenal activity, which enhances vascular tone, but complete α-adrenoreceptor blockade cannot prevent the long-lasting vasoconstriction induced by sympathetic nerve stimulation. That is why it is suggested that sympathetic nerve-mediated vasoconstriction may also be mediated by factors other than catecholamines. In this review, we aim to present the relationship between blood pressure effectors and stress altogether, along with evaluating the relationship between stress and blood pressure. In this respect, we have identified topics to explain the relationship between stress and the renin angiotensin aldosterone system, glucocorticoids, endothelial nitric oxide, endothelin-1 and L-type Ca2+ channels. Hippokratia 2015; 19 (2): 99-108.

Keywords: Acute Stress; Blood Pressure; Chronic Stress; Stress.

Figure 1. Schematic drawing demonstrating the response for acute stress. SNS: sympathetic nerve system.

Figure 2. Schematic drawing demonstrating the effects of chronic stress.

Figure 3. Schematic drawing demonstrating the effects of prolonged SNS activation. SNS: sympathetic nerve system, ACE: angiotensin converting enzyme, AngI: angiotensin I, AngII: angiotensin II, AT1-R: AngII type 1 receptor, ACTH: adrenocorticotropic hormone, ADRβ1: beta1-adrenergic receptors, cAMP: cyclic adenosine monophosphate, Ca⁺²: calcium ion.

Figure 4. Schematic drawing demonstrating the atherosclerotic effect of endothelin-1 (ET-1). ET-A: endothelin-1 receptor A, receptor PDGF: platelet-derived growth factor, FGFs: fibroblast growth factors, EGF: epidermal growth factor.