Adrenergic Receptors Lab Report

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

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

Alpha-blockers or alpha-adrenergic antagonist drugs help to decrease blood pressure and dilate blood vessels, allowing for blood to move more freely.Alpha-blockers accomplish this by either limiting or inhibiting the affects of norepinephrine, a stimulant hormone of the sympathetic nervous system. The term norepinephrine or noradrenaline works to constrict the muscles that line the interior of small veins and arteries in the body (Mayo Clinic, 2014). There are two types of alpha-receptors that are affected by norepinephrine, alpha-1 and alpha-2 receptors.Alpha-1 receptors are found throughout the body in: male reproductive organs, eyes, bladder, prostatic capsule, and more importantly blood vessels.Alpha-2 receptors exist in presynaptic nerve terminals. By blocking noradrenaline affects on alpha-1 receptors coronary arteries and veins will remain open, allowing for increased blood flow and in turn lowering blood pressure (Aschenbrenner & Venable, 2012).

In the presence of excess T3 and T4, an increase in number as well as affinity of beta-adrenergic receptors in the heart is noted. These receptors facilitate the action of "fight, flight and fright" hormones ( epinephrine, norepinephrine) which are positively chronotropic ( beat faster) and inotropic ( pump harder) to the heart. This may then lead to cardiac failure in older patients.

Experiment one tested the concentration of experimental beta blockers, and its relationship with the percent decrease in of the heart rate of the Daphnia. Our goal, was to prove that, an increased concentration of beta blockers would decrease the overall heart rate of the Daphnia being tested. Our results, established, that as the beta blocker concentration increased, so did the decrease in the heart rate of the Daphnia. Experiment two tested two unknown concentrations (A and D) and its effect on the Daphnia to see if it contained any concentration of beta blockers. The results, for concentration A showed very little effect, and concentration D seemed to have no effect on the Daphnia at all. Experiment one shows, that

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.

The use of a vasopressor in short exposure, usually no more than nine hours at a rate of .51 micrograms/kg/min. Norepinephrine, an alpha 1 and 2 receptor, is a vasoconstrictor being used to treat hypotension that is not responding to fluid replacement, in turn not regulation the mean arterial pressure. NE given to reduce the symptoms of sepsis shock due to being a Beta 1 activator. Adverse effects of NE alter heart rate or rhythm, cause angina and possible overdose if maximum dose limit is exceeded. (Girard, Opal & Ely, 2005)

Exercise 2 was separated into six parts, five of which can be seen in Table 2 and the sixth one in Table 3. Acetylcholine decreased the heart rate due to the fact that it works in the parasympathetic nervous system and increases potassium flow into the heart.

(c) Estimate the EC50 values for the effects of acetylcholine and nitroprusside in both types of arterial ring, and present these in a table.

Aldosterone stimulates the kidneys in proportional amounts of sodium intake back in the blood and the amount of potassium going out in our urine.

SOT is a non-selective, hydrophilic β -blocker which prolongs cardiac repolarization independent of its antiadrenergic action, thus representing class III antiarrhythmic properties [7]. For SOT, which has (-) and (+) conformation, it is the (-) enantiomer that possesses the majority of the β-blocking activity. However, both enantiomers of SOT share an equivalent degree of Class III antiarrhythmic potency [4]. The importance of this finding has been emphasized in the SWORD study [8] that was terminated prematurely because the optically pure (+) enantiomer that only exerts antiarrhythmic class III activity without beta-blocking effects increased mortality due to arrhythmic deaths by 65 % (p = 0.006) compared to placebo. Thus, the antiarrhythmic efficacy of SOT was increases by its the antiarrhythmic class III activity. However, beta-blockade (effected exclusively by the (-) enantiomer) appears to play an important part in both safety and efficacy of SOT

The mechanism for fall in arterial pressure after intravenous induction is multifactorial. The fall in arterial pressure after the propofol is associated with both, vasodilatation with reduced preload and afterload and myocardial depression because of the negative inotropic effect.2,14-16 This hypotension is caused by inhibition of sympathetic nervous system and impairement of baroreceptor regulatory mechanism.17 Similar to our results, Saricoaglu et al14 found that propofol was associated with significant fall in arterial blood pressure as compared to etomidate and attributed this hypotension to the negative ionotropic effect of propofol. Conversely, etomidate distinctively have the capacity to bind and stimulate peripheral alpha-2 beta adrenergic receptors with subsequent vasoconstriction18 and its lack of effect on sympathetic nervous system and baroreceptor function.2,19 These unique effects may be responsible for the haemodynamic stability after the

The renin-angiotensin-aldosterone system (RAAS) is a group of hormones that are produced sequentially in order to regulate salt-water homeostasis as well as blood pressure.5 The first enzyme, renin, is produced by the juxtaglomerular cells of the kidney when blood volume is low and is released into the bloodstream.3,5,6 Renin then catalyzes the conversion of angiotensinogen to angiotensin I.3,5,6 Angiotensin-converting enzyme (ACE), which is produced in the lungs, subsequently converts angiotensin I to angiotensin II, a more active enzyme.3,5,6 Angiotensin II has several functions. The hormone’s primary mechanism for increasing blood pressure is through the stimulation of blood vessel constriction. Furthermore, angiotensin II increases the contractility of the heart via sympathetic activation. It also stimulates anti-diuretic hormone (ADH) release, which increases water reabsorption at the collecting ducts, resulting

Introduction: The skin is the largest organ in the human body, it has many functions, for example, it helps regulate body temperature, it protects the body against microbes and other harmful substances and it allows the body to feel the sensation of touch, pain, heat and cold. The image on the right shows a cross cut section of the parts and the layers of skin; firstly the epidermis, it is the outermost layer of the skin. Then there's the 2nd layer, the dermis, which contains the connective tissue, hair follicles, sweat glands, nerves and sensory receptors.

A 20-G heparin-filled catheter (Spacelabs Medical, Inc., Redmond, WA, USA) was inserted from the right carotid artery to the left ventricle. A pressure transducer (Biolap 420F, Taimeng, Chengdu, China) was connected for hemodynamic parameters measurement. Left ventricular systolic pressure (LVSP), left ventricular enddiastolic pressure (LVEDP), and maximum rate of increase/decrease in left ventricular pressure (±dP/dtmax) were recorded throughout the experiment.