The Physiology of Blood Pressure Control
Describe the physiology of blood pressure control. Causes of Primary Hypertension may include overactivity of the SNS; overactivity of the RAAS; alterations in other neurohumoral mediators of blood volume and vasomotor tone such as ANP, BNP, and adrenomedullin; inflammation; a complex interaction involving insulin resistance and endothelial function; and obesity-related hormonal changes. identify the organ damage that can occur as a result of Hypertension. Describe the pathophysiologic process of the organ damage.
Sample Paper
Hypertension
The physiology of blood pressure control can take place both in the long and short term. When it comes to short-term management of blood pressure the autonomic nervous system kicks in, where baroreceptors detect the changes in the blood. Again, a reduction in arterial pressure is exposed by baroreceptors that trigger a sympathetic response (Seidiel & Scholl, 2017). However, it is essential to note that Baroreceptors are unable to control blood pressure in the long term. The reason is that the mechanism at hand allows the receptors to reset themselves once the blood pressure is restored. On the other hand, long-term blood pressure regulation incorporates the renin-angiotensin-aldosterone system (RAAS). The overall response is sent to act on the sympathetic stimulation, thus decreasing the kidneys’ blood flow. Similarly, the ADH manages blood pressure reduction in the long term, producing the hypothalamus to manage the condition.
On the other hand, there are instances of organ damage that take place due to hypertension. The hypertensive end-organ damage affects organs such as the heart where it causes coronary heart disease and heart failure (Monticone et al., 2018). Due to the high blood pressure, the arteries are highly affected, making them less elastic in the long run. Low elasticity decreases the blood flow and oxygen to the heart and thus causing heart disease. On the other hand, a decrease in blood flow results in chest pain commonly referred to as angina (Rubattu et al., 2015). In a nutshell, heart failure is more of a pathophysiologic state where the heart is affected via an abnormal cardiac function. Thus, the failure to pump blood at a rate commensurate with the body’s metabolism and thus a high diastolic pile-up of pressure.
References
Monticone, S., D’Ascenzo, F., Moretti, C., Williams, T. A., Veglio, F., Gaita, F., & Mulatero, P. (2018). Cardiovascular events and target organ damage in primary aldosteronism compared with essential hypertension: a systematic review and meta-analysis. The lancet Diabetes & endocrinology, 6(1), 41-50.
Rubattu, S., Pagliaro, B., Pierelli, G., Santolamazza, C., Di Castro, S., Mennuni, S., & Volpe, M. (2015). Pathogenesis of target organ damage in hypertension: role of mitochondrial oxidative stress. International Journal of Molecular Sciences, 16(1), 823-839.
Seidel, E., & Scholl, U. I. (2017). Genetic mechanisms of human hypertension and their implications for blood pressure physiology. Physiological genomics, 49(11), 630-652.
