Mean Arterial Blood Pressure

Following exposure to epinephrine, the heart was allowed to return to its resting state determined in procedure 1. This same procedure was repeated with the following chemicals: 1) Acetylcholine, 2) Atropine, 3) Calcium solution, 4) Nicotine solution, and 5) Caffeine solution.

It leads to a reduction in supine and standing blood pressure without a compensatory rise in the heart rate (reflex tachycardia). The effect of a single dose is apparent in 1-2 hours and its peak effect is 3-6 hours. The abrupt cessation of Ramipril does not produce a rapid and extreme rebound increase in blood pressure. Ramipril can be used as a therapy for heart failure as the drug has beneficial effects on cardiac haemodynamics. It results in decreased left and right ventricular filling pressures, reduced total peripheral resistance and increased cardiac

Atropine showed the only a minor increase in amplitude and period. The BPM was the detected as increase up to 30 seconds then a drop back down to 44, then the heart rate shot back up to 48 before recovering.

Epinephrine/adrenaline: Heart rate is increased by the sympathetic nervous system and the hormone adrenaline circulating in the blood via activation of cell surface receptors in

The purpose of arterial pressure and the pulse lab is to determine the effect of posture and exercise on systolic and diastolic pressure and the heart rate. And also in order to find the differences in the reading taken under these condition compares to the baseline reading. The Sphygmomanometer and stethoscope are used to measure the systolic and diastolic blood pressure, counting the beat on the radial artery will give the reading for pulse rate and by using the lab scribe software and IWX214, the blood pressure will be measured. In the heart, the aorta and the carotid arteries have baroreceptors and the chemoreceptors that identify the changes in arterial pressure and the changes in

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).

Acetylcholine is found at the peripheral nervous system and synapses in the central nervous system within the human body. Acetylcholine is an excitatory neurotransmitter that conducts electrical impulses, allowing nerve cells to communicate with muscle cells and generate muscle contractions. However, acetylcholine produces an inhibitory effect in cardiac muscle. (Waymire, 1997) Therefore, once the Daphnia are exposed to acetylcholine, their heart rate is expected to decline. In contrast, epinephrine, also known as adrenaline, is a hormone which binds to the beta adrenergic receptors in the heart leading to increases in the firing rate of the pacemaker cells. (Meyers, 2011) Therefore, the Daphnia’s heart rate is expected to increase with exposure to

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,

Though data from vagal stimulation was disregarded, it is still important to mention the responses that should have been elicited had the vagus nerve been stimulated properly. The vagus nerve (cranial nerve X) is a part of the parasympathetic nervous system and reduce heart rate when given enough electrical stimulation. Vagal escape occurs when the vagus nerve has been stimulated to the point of the nerve ceasing to repolarize, and then resuming sending action potential for heartbeat. The result is a cease or slowing of heart rate temporarily, and then heart rate starting up again. When atropine is applied to the heart along with vagal stimulation, the atropine blocks any response the vagus nerve should send (Sarnoff et al,

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.

Shearing forces acting on the vascular endothelium generated by blood flow causes a release of calcium and subsequent cNOS (cyclic nitric oxide synthase) activation. Therefore, increases in blood flow stimulate NO formation (flow-dependent NO formation). Nitric oxide then causes independent vasodilation by inhibiting vasoconstrictor influences of phenylephrine and alters its potency and contractile effect. (Richard E. Klabunde. 2010)

A cuff sphygmomanometer in the brachial artery has been accepted as a routine method of blood pressure measurement but it is actually higher than corresponding central blood pressure measured from aorta and carotid artery. However, many evidence suggests that central blood pressure is better related to the risk of cardiovascular events than is brachial pressure [5]. Vaccarino et al. reported that the increased central pulse pressure about 10 mmHg increases a heart failure risk about 14 %, coronary heart disease about 12 % and cause mortality about 6 % of the population older than 65 years [39]. To monitor the hypertensive condition, central blood pressure values i.e. systolic, diastolic blood pressure and augmentation index are used as gold standard parameters. PWV is also a useful marker of target organ damage such as heart, brain, aorta and kidney in hypertensive patients [16]. In addition, treatment decisions on central pressure, rather than brachial pressure, is more likely to have important clinical application for the diagnosis and proper management of hypertension because anti-hypertensive drugs have differential effects on brachial and central pressure[40]. Recently, the 2013 hypertension guidelines has added aortic PWV as a recommended test for detecting large artery stiffening associated with

Basically, arterial blood pressure (BP) is directly proportional to the product of blood flow (cardiac output, CO) and the resistance to passage of blood through pre-capillary arterioles (peripheral vascular resistance, PVR) Hypertension can be caused by either an increase in Cardiac Output (CO) or by an increase in Peripheral Resistance (PR)

amount of pressure exerted on arterial walls in the patient’s heart. Blood pressure is measured in