Apart form adrenaline, what other hormones in humans affect the cardiovascular system?
I want to study the relationship between addressing one's fears and the effect it has on the cardiovascular system, but I want to make the increased heart rate was due to adrenaline. Thanks!
Best answer:
Answer by TOWFEEQ UMAR
Neural and Hormonal Affects
There are two different factors involved in heart rate management: intrinsic and extrinsic controls. Intrinsic regulation of heart rate is the result of the unique nature of cardiac tissue - it is self-regulating and maintains it's own rhythm without direction. Extrinsic controls are those that come from both hormonal responses as well as the commands from the nervous system: the central nervous system and the autonomic nervous system. Extrinsic regulation can cause the heart rate to change rapidly because of chemicals that circular in the blood or by directaction of nerves that go to the heart.
A good example of this is to measure heart rate changes when certain words or emotions are said or felt without a muscle contracting. Say the words, "we are going tohave a surprise test today" and watch heart rate extrinsically increase. Put on a heart rate monitor and sitting completely still watch a movie and watch heart rate jump during a car chase or action thriller. There is no cardiovascular or cardio respiratory change as a result of this change in heart rate; it's simply the affect on the heart ofchemicals and nerves responding to an external experience.
The cardiovascular control center for the body is located inthe ventro-lateral medulla. Here heart rate slows if activated by the cardio inhibitory center in the medulla or speeds up if activated by the cardio accelerator.
From this site, the two channelsof the autonomic nervous system originate the sympathetic and parasympathetic components. The sympathetic components increase heart rate by releasing the neural hormone catecholamines - epinephrine and norepinephrine. These hormones are cardio accelerators. Acceleration of theheart rate is called tachycardia.
The parasympathetic nervous system located in the brain stem and upper or sacral portion of the spinal cord slowsheart rate. The parasympatheticcomponents decrease heart rate. These neurons release the neurohormone acetylcholine, which inhibits heart rate. The slowing of heart rate is called bradycardia.
The combination of the neural and chemical components regulates heart rate and other heart functions. When you begin to exercise in heart zones1-3, heart rate increases because parasympathetic (cardioinhibitory) stimulation stops. During more strenuous exercise, heart zones 3-5, the heart rate increase occurs by direct activation of the sympathetic cardioaccelerator nerves.
Exercise excites the relationshipbetween the sympathetic accelerators and the parasympathetic depressor neurons. This change in the balance in their activity called tonic activity leads to more involvement of the vagus nerves. The vagus nerves carry about 80% of the parasympathetic fibers, those responsible for slowing heart rate. With increased vagal dominance, heart rate values change and slow. One of the training effects is the slowing of resting and ambient heart rates. This is the result of the effect of fitness on the tonic activity and the favoring of greater activity by the vagus nerves to slow heart rate. Theseadaptations following zone 1-3 or aerobic training occur to those who are sedentary and begin and exercise program as well as those who maintain one. This is one of the benefits of training, a significant resting bradycardia.
The central nervous system plays the greatest role in controlover heart rate during exercise. When you start a movement pattern, the central nervous system sends impulses through the cardiovascular center in the medulla. There is a coordinated and quick response of both the heart and the blood vessels to change blood pressure, tissue perfusion to respond to the requirements.
A good example of the central command involvement is with anticipatory heart rate. Before an event begins, if the individual anticipates with excitement and enthusiasm the event, heart rate increases dramatically without any muscular involvement. Anticipatory heart rate or your heart rate immediately before exercising in one experiment averaged 148 bpm when the announcer started giving starting commands to a group of sprinters. In this experiment, heart rates increased 140% in anticipation of the starting of this 60-yard dash. In fact, the body that the body increases heart rate in anticipation is good because it provides for the rapid mobilization of it's bodily reserves by revving the body's engine. Research shows that the longer the event, the lower the anticipatory heart rate changes.
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Hormones have an influence on many tissues and organs, including the cardio-vascular system (CVS). Depending on their activity on CVS, they can be divided into 4 groups: having hypertensive or hypotensive influence and chronotropic positive or negative action. Endocrine regulation in CVS may occur in many ways. Apart from hormones usually connected with CVS regulation, other more recently, discovered ones can act on it. A few of these act directly through specific receptors in heart or vessel wall cells, whereas some act indirectly - stimulating other neuroendocrine factors. Additionally, novel mechanisms of signal transduction have been discovered for steroid and thyroid hormones, which are independent of gene transcription regulation and are - known as "nongenomic". Hormones which increase blood pressure include: urotensin II, endothelins, angiotensin II, catecholamines, aldosterone, antidiuretic hormone, glucocorticosteroids, thyroid hormones, growth hormone and leptin. On the other hand, blood pressure can be decreased by: natriuretic peptides, the calcitonin gene-related peptide (CGRP) family, angiotensin 1-7, substance P, neurokinin A, ghrelin, Parathyroid hormone-related protein (PTHrP), oxytocin, and, sex hormones. Hormones which when appearing in excess increase the heart rate are: catecholamines, endothelins, glucocorticosteroids, thyroid hormones, leptin and PTHrP. Those which decrease the heart rate include: natriuretic peptides, substance P, neurokinin A, oxytocin, angiotensin 1-7. This paper describes the contemporary view of the functions of hormones which act on the vessel tree and heart. The particular effect of mediator depends on many circumstances i.e.: hormone concentration, receptor type. It may also undergo contraregulation. The majority of those hormones play an important role in the pathogenesis of CVS diseases', which can result in the development of new medicines
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