The heart and blood vessels work together in complex ways to deliver an adequate amount of blood

to all parts of the body (Ivy and Bailey, 2014). The cardiovascular system is regulated by a variety of
stimuli, including changes in blood volume, electrolytes, hormones, osmotic pressures, drugs,
kidneys, adrenal glands, and many more (Ivy and Bailey, 2014). Stroke volume is the amount of
blood pumped from the heart after contraction (Lohmeier, 2001). This is the difference between
end-diastolic volume and end-systolic volume, it increases with increasing contractility, increasing
preload, and decreasing afterload (Lohmeier, 2001).

Several mechanisms help regulate arterial pressure; baroreceptor reflex and antidiuretic hormone
(Dampney et al., 2002). Baroreceptors are a type of mechanoreceptor that is activated by the
extension of blood vessels (Lohmeier, 2001). This sensory information is transmitted to the central
nervous system and used to influence peripheral vascular resistance and cardiac output (Dampney
et al., 2002). Two forms of baroreceptors are located within the high-pressure arterial system.
Carotid baroreceptors respond both to rising and falling blood pressure and send afferent signals
through the glossopharyngeal nerve (Dampney et al., 2002). The aortic arch baroreceptor responds
only to elevated blood pressure and sends signals through the vagus nerve (Dampney et al., 2002).
The main function of the antidiuretic hormone is to increase the reabsorption of free water in the
collecting ducts of the renal nephrons, causing an increase in plasma volume and blood pressure
(Zimmerman and Davisson, 2004). Antidiuretic hormone at high concentrations has also been shown
to cause moderate vasoconstriction, increased peripheral resistance, and increase blood pressure
(Zimmerman and Davisson, 2004).

The cardiac cycle represents the path of blood through the heart (Mancia et al., 1983). It follows in
the ascending order of atrioventricular contraction, mitral valve closure, isotonic stage, aortic valve
opening, ejection phase (rapid and reduced ejection), left ventricular drainage, aortic valve closure,
isotonic relaxation, mitral valve opening, and filling stage (rapid and reduced filling) on the left
ventricle (Mancia et al., 1983).

Through their effects on adrenergic and dopamine receptors, epinephrine and dopamine regulate
blood pressure and cardiovascular function (Desir et al., 2012). Neuronal and extra-neuronal tissues
are involved in the metabolism of these compounds, with monoamine oxidase being the intracellular
enzyme responsible for breakdown (Desir et al., 2012). Adrenaline shortens isometric contraction
phases, accelerates contraction speed, increases left ventricle systolic emptying, increases the first
and the second heart sounds, lowers diastolic pressure, increases cardiac output, increases pulse
pressure amplitude, and the heart usually increases as a result (Xu et al., 2005).

Propranolol lowers cardiac output by reducing the cardiac component of pressor stimuli (Dowd,
2014). This, in turn, allows the baroreceptors to regulate blood pressure at a lower level (Dowd,
2014). Normally, the effect of norepinephrine and epinephrine on the heart is induced by
competitively blocking beta-1 and beta-2 adrenergic stimulation (Dowd, 2014). In cardiac myocytes,
beta-1 adrenergic receptors are present (Paravastu, Mendonca and Da Silva, 2013). When they are
blocked, there is an overall reduction in the workload of the heart, which in turn leads to a decrease
in oxygen demand and remodelling (Paravastu, Mendonca and Da Silva, 2013). When beta-2
receptors are activated, adenosine monophosphate (AMP) increases, which activates protein kinase
A, resulting in relaxation of smooth muscle cells throughout various organs and vessels (Paravastu,
Mendonca and Da Silva, 2013). This blocks the receptors that epinephrine would potentially be to in
the lungs, or endothelium, resulting in a small amount of vasoconstriction (Aronow, 2010). This can
make the use of emergency epinephrine problematic in asthmatics (Aronow, 2010).
As well as reducing arterial pressure, propranolol reduces triglycerides and cholesterol (Aronow,
2010). Having low blood pressure is achieved by blocking the sympathetic receptors in the heart,
which are responsible for regulating blood pressure (Aronow, 2010). In addition to lowering blood
pressure, propranolol reduces the strength of heart contractions, thus reducing the heart's need for
oxygen (Weber and Reinmuth, 1972). Propranolol, by reducing the demand for oxygen in the heart
muscle, helps in treating heart pain because it reduces the oxygen demand in the heart muscle
(Weber and Reinmuth, 1972).
 

When insulin-induced hypoglycaemia is induced in diabetics, propranolol impairs glucose recovery

by blocking epinephrine’s inhibition of glucose utilisation (Popp et al., 1984). However, in normal,
propranolol’s effect is largely due to its blocking of epinephrine-induced hepatic glucose production
(Popp et al., 1984). The risk of glucose control being affected by beta-blockers is minimal in
nondiabetics (Popp et al., 1984). Insulin-dependent diabetics may experience prolonged, enhanced,
or altered hypoglycaemia symptoms while noninsulin-dependent diabetics appear to be more at risk
of hyperglycaemia (Popp et al., 1984). In spite of lower free fatty acids and higher lipoprotein lipase
activity in adipose tissue, there is a significant reduction in lipoprotein lipase activity in muscle during
propranolol treatment, resulting in a pronounced increase in serum triglyceride levels (William-
Olsson et al., 2009).

Patients with diabetes taking propranolol show an increase in diastolic pressure and a significant fall
in heart rate (William-Olsson et al., 2009). The treatment of hypertension in diabetes-prone to
hypoglycaemic attacks should not consist of beta-blockers since propranolol may cause a sharp rise
in blood pressure (William-Olsson et al., 2009). The use of beta-blockers is beneficial in diabetic
patients who have a 2 to 4-fold greater risk of cardiac heart disease and stroke (Yuhei Kawano,
Hitoshi Abe, Shunichi, 1999). Consequently, these drugs will likely be prescribed frequently to
diabetics (Yuhei Kawano, Hitoshi Abe, Shunichi, 1999). The majority of physiological responses to
sympathetic activation are mediated by norepinephrine, while sweating is mediated by
acetylcholine, which activates nicotinic receptors on glands (Yuhei Kawano, Hitoshi Abe, Shunichi,
1999). In diabetic patients, beta-blocker is not recommended because of the possibility of worsened
glucose and lipid metabolism, as well as more severe hypoglycaemic attacks (William-Olsson et al.,
2009).

References  
Insert references here using journal articles and textbooks only. Use Harvard, APA,
Numbered or Vancouver.

 
 Aronow, W.S. (2010). Current role of beta-blockers in the treatment of hypertension.
Expert Opinion on Pharmacotherapy, [online] 11(16), pp.2599–2607. Available at:
https://doi.org/10.1517/14656566.2010.482561 [Accessed 11 Jan. 2022].

Dampney, R., Coleman, M., Fontes, M., Hirooka, Y., Horiuchi, J., Li, Y-W., Polson, J., Potts, P.
and Tagawa, T. (2002). Central Mechanisms Underlying Short- And Long-Term Regulation Of
The Cardiovascular System. Clinical and Experimental Pharmacology and Physiology, [online]
29(4), pp.261–268. Available at: https://doi.org/10.1046/j.1440-1681.2002.03640.x
[Accessed 10 Jan. 2022].

Desir, G.V., Tang, L., Wang, P., Li, G., Sampaio‐Maia, B., Quelhas‐Santos, J., Pestana, M. and
Velazquez, H. (2012). Renalase Lowers Ambulatory Blood Pressure by Metabolizing
Circulating Adrenaline. Journal of the American Heart Association, [online] 1(4). Available at:
https://doi.org/10.1161/JAHA.112.002634 [Accessed 11 Jan. 2022].

Dowd, S.M. (2014). Everything You Need to Know About TMSEverything You Need to Know
About TMS. PsycCRITIQUES, 5959(5050).

Ivy, J.R. and Bailey, M.A. (2014). Pressure natriuresis and the renal control of arterial blood
pressure. The Journal of physiology, [online] 592(18), pp.3955–67. Available at:
https://doi.org/10.1113/jphysiol.2014.271676 [Accessed 9 Jan. 2022].

Lohmeier, T. (2001). The sympathetic nervous system and long-term blood pressure
regulation. American Journal of Hypertension, [online] 14(11), pp.S147–S154. Available at:
https://doi.org/10.1016/S0895-7061(01)02082-9 [Accessed 10 Jan. 2022].

Mancia, G., Ferrari, A., Gregorini, L., Parati, G., Pomidossi, G., Bertinieri, G., Grassi, G.,
Rienzo, M. di, Pedotti, A. and Zanchetti, A. (1983). Blood Pressure and Heart Rate
Variabilities in Normotensive and Hypertensive Human Beings. Circulation research, 53(1),
pp.96–104.

Paravastu, S.C.V., Mendonca, D.A. and Da Silva, A. (2013). Beta blockers for peripheral
arterial disease. Cochrane Database of Systematic Reviews. [online] Available at:
https://doi.org/10.1002/14651858.CD005508.pub3 [Accessed 11 Jan. 2022].

Popp, D.A., Tse, T.F., Shah, S.D., Clutter, W.E. and Cryer, P.E. (1984). Oral Propranolol and
Metoprolol Both Impair Glucose Recovery from Insulin-induced Hypoglycemia in Insulin-
dependent Diabetes Mellitus. Diabetes Care, [online] 7(3), pp.243–247. Available at:
https://doi.org/10.2337/diacare.7.3.243 [Accessed 11 Jan. 2022].

Weber, R.B. and Reinmuth, O.M. (1972). The treatment of migraine with propranolol.
Neurology, 22(4), pp.366–369.
William-Olsson, T., Fellenius, E., Björntorp, P. and Smith, U. (2009). Differences in Metabolic
Responses to β-Adrenergic Stimulation after Propranolol or Metoprolol Administration. Acta
Medica Scandinavica, [online] 205(1-6), pp.201–206. Available at:
https://doi.org/10.1111/j.0954-6820.1979.tb06031.x [Accessed 11 Jan. 2022].

Xu, J., Li, G., Wang, P., Velazquez, H., Yao, X., Li, Y., Wu, Y., Peixoto, A., Crowley, S. and Desir,
G.V. (2005). Renalase is a novel, soluble monoamine oxidase that regulates cardiac function
and blood pressure. Journal of Clinical Investigation, [online] 115(5), pp.1275–1280.
Available at: https://doi.org/10.1172/JCI24066 [Accessed 11 Jan. 2022].
YUHEI KAWANO, HITOSHI ABE, SHUNICHI (1999). Effects of Propranolol on Cardiovascular
and Neurohumoral Actions of Alcohol in Hypertensive Patients. Blood Pressure, [online] 8(1),
pp.37–42. Available at: https://doi.org/10.1080/080370599438374 [Accessed 11 Jan. 2022].

Zimmerman, M.C. and Davisson, R.L. (2004). Redox signaling in central neural regulation of
cardiovascular function. Progress in Biophysics and Molecular Biology, [online] 84(2-3),
pp.125–149. Available at: https://doi.org/10.1016/j.pbiomolbio.2003.11.009 [Accessed 10
Jan. 2022].