CARDIOVASCULAR AND RENAL CONTROL OF ARTERIAL BLOOD

PRESSURE

INTRODUCTION

Pumping oxygenated blood to the body and deoxygenated blood to the lungs while adapting to
rapidly changing body tissues requirements, the human heart and its functions are under tightly
regulated control, being influenced by the autonomic nervous system (ANS), the renal system,
and the endocrine system (Gordan, Gwathmey, & Xie, 2015). The fundamentals of arterial
blood pressure (BP) regulation have been long established and it is now well known that BP is
positively related to cardiac output, as well as to total peripheral vascular resistance (Gordan et.
al., 2015). These aforementioned systems work in harmony to maintain arterial pressure in
normal physiological state as well as in heart-associated pathologies (Gordan et. al., 2015). This
essay firstly addresses the role of the arterial baroreceptor and chemoreceptor reflexes as part
of the cardiovascular system's short-term control of BP, after which it discusses the role of the
renal system in the long-term regulation through the renin-angiotensin-aldosterone pathway.
Finally, the different hormones acting to maintain BP homeostasis are briefly mentioned in the
last part of the current work.
CARDIOVASCULAR SYSTEM CONTROL OF BLOOD PRESSURE

The cardiovascular system, subjected to autonomic nervous system (ANS) control, ensures
arterial pressure homeostasis via mechanical or pressure receptors, baroreceptors, as well as
via chemical receptors, chemoreceptors (Boron & Boulpaep, 2016). Baroreceptors provide
information about arterial BP, whilst chemoreceptors convey information about the partial
pressures of oxygen and carbon dioxide in the blood, as well as pH (Purves et. al., 2001). These
sensors, using afferent neural pathways influence the sympathetic and parasympathetic
efferent activity related to cardiovascular control (Gordan et. al., 2015).

BARORECEPTORS

Situated in the heart and the major systemic arteries in the carotid sinus and the aortic arch,
the baroreceptors are high-pressure loci pivotal in the short term control of BP (Boron &
Boulpaep, 2016). Activation due to the stimulation of their nerve endings by the stretching of
the blood vessels walls leads to a negative-feedback mechanism controlling and integrating BP
(Purves et. al., 2001). Thus, an increase in systemic arterial pressure leads to internal carotid
artery wall distension and afferent signals transmission via the vagus nerves, Hering’s nerves,
and glossopharyngeal nerves to the medullary cardiovascular centre (Boron & Boulpaep, 2016).
The two distinct subdivisions within this centre, the vasomotor area and the cardio-inhibitory
area, both participate in cardiovascular homeostasis coordination, the former being negatively
modulated by baroreceptors input (Boron & Boulpaep, 2016). The baroreflex efferent neural
pathways comprise both the sympathetic and parasympathetic divisions of the ANS (Boron &
Boulpaep, 2016). Thus, increased BP promotes efferent sympathetic signals attenuation to the
heart and the vascular smooth muscle, followed by parasympathetic output stimulation
(Kougias, Weakley, Yao, Lin , & Chen, 2010). The effects of this integrating pathway have been
shown to be vasodilation, reduced heart rate and strength of contraction, and thus a drop in
BP, re-establishing homeostasis (Kougias et. al., 2010). Conversely, a drop in BP leads to
insufficient stretching of the pressure receptors, followed by stimulation of the vasomotor area
in the medullary cardiovascular centre, increased sympathetic stimulation and thus
vasoconstriction and cardiac output augmentation, all mechanisms leading to a rise in BP
toward normal values (Kougias et. al., 2010).

Furthermore, a physiological phenomenon known as “baroreceptor resetting” plays a

significant role in the minute-by-minute control exerted by baroreceptors, their mechanism of
action being adjusted to a higher baseline BP after being exposed to it for an extended period
of time (Kougias et. al., 2010). Also, evidence shows that there are two distinct resetting
mechanisms: acute and chronic baroreceptor resetting (Kougias et. al., 2010). The first form
which has been shown to be stable for at least one hour and completely reversible, is triggered
by prompt alterations in the pressure to which the receptors are exposed for a brief duration
such as 20 minutes or less (Kougias et. al., 2010). The second form is characterised by
decreased baroreceptor sensitivity and these changes are not easily reversible (Kougias et. al.,
2010). Therefore, the baroreflex, although pivotal in the continuous monitoring and controlling
of BP, induces an effect easy to diminish after prolonged exposure to increased systemic
pressure (Kougias et. al., 2010).

CHEMORECEPTORS

Baroreceptors and the baroreflex are different from chemoreceptors, a unique group of
specialised cells situated in the carotid and aortic bodies (Hall, 2010). Their role in regulating BP
is according to continually changing oxygen and carbon dioxide partial pressures, as well as
hydrogen ions surplus in the blood (Kougias et. al., 2010). As a result of their abundant blood
flow and sensing properties of minute arteriovenous differences for Po2, PCO2 and pH, carotid
bodies monitor the composition of arterial blood, increasing signaling frequency to the afferent
sinus nerve (Gordan et. al., 2015). The main signal triggering a rise in sensory fibres firing
frequency is peripheral chemoreceptors sensing of a reduced oxygen partial pressure (Hall,
2010). Afferent signals from the carotid and aortic bodies transmit impulses via the Hering’s
and the glossopharyngeal nerves to the vasomotor centre in the brain, as well as to the nucleus
tracts solitarii (Gordan et. al., 2015). Hence, the afferent signals relayed from the
chemoreceptors positively modulate the vasomotor centre, which further promotes increased
sympathetic stimulation and thus vasoconstriction, elevated heart rate and stroke volume and
BP elevation to normal ranges (Gordan et. al., 2015). However, since O2 partial pressure
fluctuations in humans are not considerably large to negatively impact BP, the peripheral
chemoreceptors are activated mainly in severe hypoxia conditions (Hall, 2010). Furthermore,
the central chemoreceptors located in the medulla oblongata differ from peripheral sensors,
being sensitive to low brain pH normally indicating a high arterial CO2 partial pressure (Boron &
Boulpaep, 2016). Consequently, detection of a reduced Po2 by peripheral chemoreceptors and
a significant Pco2 by central chemoreceptors leads to increased vasoconstriction and thus
chemoreceptor regulation of BP (Boron & Boulpaep, 2016).

Noteworthy, regarding the correlation between the cardiovascular and renal systems, several
lines of evidence have suggested that baroreceptors may bestow long-term BP control by
causing either a decrease or increase in the sympathetic nerve activity of the kidneys (Hall,
2010). Depending on the situation, rises or drops in the excretion of sodium and water by the
kidneys leads to a decline or elevation in blood volume, respectively (Hall, 2010). As a result,
normal arterial pressure is reinstated, a process which emphasises the significance of the
interaction between baroreceptors and the renal system, more specifically the body fluid and
pressure regulation control mechanisms (Hall, 2010).

RENAL SYSTEM CONTROL OF BLOOD PRESSURE

In contrast to the short-term regulation previously discussed, the renal-body fluid system is
considered to play a central role in the long-term regulation of BP, evidence pointing to
increased urinary output concomitantly with increasing arterial pressure, and thus to the
kidneys' efficacy in returning pressure back to normal (Hall, 2010). The multiple mechanisms
employed by the kidneys to maintain BP homeostasis finely balance fluid intake and output,
using the renin-angiotensin-aldosterone system (RAAS), as well as antidiuretic hormone (ADH)
and atrial natriuretic peptide hormone (Hall, 2010).

RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

Firstly, when BP decreases below the minimal normal value, the kidneys release renin, a
protease initially synthesised and stored as an inactive substrate in the juxtaglomerular (JG)
cells proximal to the renal afferent arterioles (Chopra, Baby, & Jacob, 2011). Renin then acts on
angiotensinogen to release angiotensin I, a mild vasoconstrictor which is further modified in the
lungs by angiotensin converting enzyme (ACE) to Angiotensin II (Chopra et. al., 2011). The latter
has two main effects that participate in the elevation of arterial pressure (Hall, 2010). Firstly,
angiotensin II is a significantly powerful arteriolar vasoconstrictor, inducing an increase in the
total peripheral resistance (TPR) and thus, elevated systolic and diastolic arterial pressure
(Gordan et. al., 2015). Secondly, it stimulates the adrenal glands to secrete aldosterone, acting
through the extracellular fluid (ECF) volume system to diminish water and salt excretion by the
kidneys, leading to an elevation in the ECF volume and thus, to increased BP (Gordan et. al.,
2015). The pivotal function of the RAAS is to maintain ECF volume and BP within normal range
irrespective of the amount of dietary salt intake (Hall, 2010). In case of elevated salt intake, ECF
volume and arterial pressure increase, leading to increased blow flow to the kidneys, decreased
renin synthesis and secretion which in turn leads to a decline in salt and water retention rate by
the kidneys (Hall, 2010). Thus, the RAAS acts through a negative feedback mechanism to return
the ECF volume and BP to normal (Hall, 2010). Conversely, when salt intake is very low, the
RAAS acts through the same system to increase and restore normal pressure (Hall, 2010).
ANTIDIURETIC HORMONE

Secondly, the antidiuretic hormone, also called vasopressin is synthesised in hypothalamic

nerve cells and transported to the posterior pituitary gland from where it is liberated into the
blood (Chopra et. al., 2011). Multiple lines of evidence point to ADH as a significantly more
powerful vasoconstrictor than angiotensin II, as well as to its role on elevating water
reabsorption from the renal tubules into the blood by making the collecting ducts more water
permeable, thus increasing BP (Chopra et. al., 2011).

ATRIAL NATRIURETIC PEPTIDE

Thirdly, another hormone that acts to reduce arterial BP is the atrial natriuretic peptide (ANP),
released as a result of atrial fibres overstretch (Gordan et. al., 2015). ANP acts on the kidneys
causing slight increases in the glomerular filtration rate and thus promoting sodium and water
excretion (Hall, 2010). Furthermore, it inhibits the synthesis and secretion of angiotensin II,
aldosterone, and ADH, decreasing angiotensin II-mediated vasoconstriction and thus reducing
BP to normal values (Hall, 2010).

CONCLUSION

In summary, as previously discussed, the cardiovascular and renal systems have crucial roles in
establishing and maintaining BP homeostasis as they both function under nervous and
endocrine control as well as display hormonal effects (Hall, 2010). The short-term BP regulation
is mainly controlled by baroreceptors as well as by chemoreceptors by adjusting cardiac output
and blood vessel diameter (Hall, 2010). Furthermore, long term BP regulation is controlled by
the kidneys via RAAS, which complements the cardiovascular system by adjusting fluid balance
and arteriolar wall wideness (Hall, 2010). Additionally, ADH and ANP participate in BP elevation
and decrease, respectively by influencing water reabsorption and filtration rates (Hall, 2010).
Lastly, multiple factors have been shown to influence the harmonious interaction between the
above discussed systems by affecting BP regulation (Hall, 2010).
REFERENCES

Boron, W., & Boulpaep, E. (2016). Medical physiology: a cellular and molecular
approach. Philadelphia, PA : Saunders/Elsevier

Chopra, S., Baby, C., & Jacob, J. J. (2011). Neuro-endocrine regulation of blood
pressure. Indian Journal of Endocrinology and Metabolism, 15(4), S281–
S288. doi.org/10.4103/2230-8210.86860

Gordan, R., Gwathmey, J. K., & Xie, L.-H. (2015). Autonomic and endocrine control of
cardiovascular function. World Journal of Cardiology, 7(4), 204–214.
doi.org/10.4330/wjc.v7.i4.204

Hall, J. and Guyton, A. (2015). Guyton and Hall Textbook Of Medical Physiology.
Philadelphia: Elsevier

Kougias, P., Weakley, S. M., Yao, Q., Lin, P. H., & Chen, C. (2010). Arterial
baroreceptors in the management of systemic hypertension. Medical
Science Monitor : International Medical Journal of Experimental and
Clinical Research, 16(1), RA1–RA8.
Purves, D., Augustine, G.J., Fitzpatrick, D. (2001). Neuroscience. Sunderland (MA):
Sinauer Associates. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK10799/

Raven, P. B., & Chapleau, M. W. (2014). Blood Pressure Regulation XI: Overview and Future
Research Directions. European Journal of Applied Physiology, 114(3), 579–586.
doi.org/10.1007/s00421-014-2823-z