Blood Pressure Regulation

Insufficient cardiac output causes compensatory mechanisms work to improve cardiac output. They include, sympathetic nervous system stimulation, Renin=angiotensin system activation, other chemical responses, and myocardial hypertrophy.

John’s long standing Hypertension causes his heart to work harder, putting more strain on his heart and arteries. In order to achieve a gradient in pressure by which blood flows from an area of higher pressure to one of lower pressure, the left ventricle must exceed the increased pressure in the arterial system (Ref).

When beta-1 receptors are turned on it leads to elevated heart rate and increased contractual force. Beta-blockers are medications used in the treatment of high blood pressure.These medications inhibit the negative effects caused by the sympathetic nervous system on the heart muscle. They act by capping off beta-receptors, and thus inhibit the stimulating affects on the heart caused by adrenaline (Aschenbrenner & Venable, 2012). The medication in-effect lowers blood pressure, by decreasing contractual force on the myocardium and reducing heart beat (Mayo Clinic,

Blood pressure in our blood vessels is monitored by the baroreceptors. These receptors send messages to the cardio regulatory center of the medulla oblongata to regulate our blood pressure every minute. In order for blood to be delivered to all organs and tissues, our cardiovascular system must always maintain adequate blood pressure. If the blood pressure drops too low, these organs will not receive an adequate of nourishing blood. Also if the pressure goes too high, the walls of the arteries will stretch and increased activity within the baroreceptor, information will then be sent through the nerves to the cardio regulatory center within the medulla which will responds by initiating the mechanisms that decrease the blood pressure to a normal

An organ bath experiment was carried out to examine different types of antagonistic (competitive reversible (CRA), non-competitive (NCA), and physiological antagonisms) mechanisms for regulating the VSM tone by using NA with prazosin (Praz), serotonin (5HT) with methysergide (Meth) and verapamil (Ver), and KCl with carbachol (Carb) on isolated rat aorta tissue. The hypothesis is the CRA mechanism will reach max contraction, but higher concentration of agonist is needed to reach max contraction in presence of antagonist, the NCA mechanism will show decrease in max contraction of agonist with presence of antagonist, and physiological antagonism will show relaxation of tissue due to the action of antagonist during presence of agonist.

In periods of extreme stress, the sympathetic nervous system will override autoregulation. An increase in sympathetic flow to the kidney will result in what two important effects that will aid maintenance of blood pressure?

Body: the regulation tof blood pressure. When your blood pressure increases, it is detected by the recepters in your blood vessels that sence the resistance of blood flow against the walls if the vessel. The receptors send a message to your brain, which sends a message to your heart and blood vessels. Your heart rate decreases and your blood vessels expand in diameter, which together decreases your blood

The PNS decreases heart rate by transmitting its impulses onto long, myelinated preganglionic neurons that trigger the release of ACh onto nicotinic cholinergic receptors found on the postganglionic cell. The impulse then travels along short, unmyelinated cholinergic postganglionic neurons, and triggers the release of ACh onto muscarinic cholinergic receptors found on the effector target cells. The speed and duration of response by the PNS is quicker because most of its axonal journey is done upon long myelinated fibers. The PNS release of ACh can also be easily broken down by acetycholinesterase, so its effect only last for a short period of time. The speed and duration of response by the SNS is slower and longer due to most of its axonal journey being done upon long

In an effort to increase cardiac output, the sympathetic nervous system is activated, through baroreceptors in the aortic arch, as an early compensatory mechanism which provides inotropic support and maintains cardiac output (Cadwallader, 2013; Yelle & Chaudhry, 2016). These compensatory mechanisms include increased heart rate, myocardial remodeling, and increased fluid volume. Chronic sympathetic activation eventually increases the stress placed on the heart and causes further weakening in cardiac function (Markaity, 2012; Yelle & Chaudhry, 2016).

There is a complex interrelationship among the cardiovascular system, the central nervous system (Na+, appetite and thirst regulation), the kidneys, and the tissue capillary beds distribution of extracellular fluid volume). Any change at any of these sites affects the function at other sites. There is a basic law of kidneys that Na+ excretion is directly proportional to mean arterial blood pressure (MABP). A marginal increase in MABP causes significant increase in Na+ excretion.

MAP. Cardiac mechanisms play a minor role in the regulation of blood pressure. So when

When the heart begins to fail, mechanisms are activated to compensate for the impaired function and maintain the cardiac output. The primary compensatory mechanisms are Frank –Starling mechanism, neuroendocrine responses including activation of the sympathetic nervous system and the renin- angiotensin-aldosterone system, and ventricular hypertrophy. Decreased cardiac output initially stimulates aortic baroreceptors, which in turn stimulate the SNS. SNS stimulation produces both cardiac and vascular responses through the release of norepinephrine. Norepinephrine increases heart rate and contractility by stimulating cardiac beta- receptors. Cardiac output improves as both heart rate and stroke volume increase. Norepinephrine also causes arterial

A neurotransmitter is a chemical that is released in order to send a signal to another neuron across a synapse. During this experiment acetylcholine was used and it is a neurotransmitter that is released from all parasympathetic postganglionic fibers (Sherwood,2016). The main function of acetylcholine is the activation of skeletal muscles and glandular functions in the endocrine system. Another neurotransmitter utilized was epinephrine. Epinephrine is the primary hormone that prepares the body for fight or flight responses and regulates arterial blood pressure in situations with adrenaline (Medicine.net, 2017). Although not necessarily a neurotransmitter, atropine sulfate was used in this study as well and it does closely effect acetylcholine. More specifically, atropine sulfate is a parasympatholytic agents that interacts with muscarinic receptors on effector cells which then prevents acetylcholine form binding to the receptor site (Kovalcuka et al., 2015). Baroreceptors also played a key role within this experiment. The primary role of baroreceptors is to sense pressure changes and to respond to change of tension in the arterial wall which helps in regulation of blood

stimulates the atrium to contract forcing blood through the valves to the ventricles. The AV

There are three systems that play an essential part in homeostatic response to intravascular volume reduction, these include; sympathetic nervous system, cardiovascular system, and neuroendocrine system. Adrenaline, noradrenaline, angiotensin II, and antidiuretics hormones assist to sustain cardiac output (CO) and sufficient tissue perfusion to the brain and the heart. Compensated, decompensated and irreversible are the 3 phases of hypovolaemic shock. Compensated shock phase is when there is a decrease in blood pressure identified by baroreceptors located in the aortic arch and carotid sinus that stimulate sympathetic output. Increased levels of catecholamines create an effect of increased heart rate, myocardial contractility, and vasoconstriction