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Experimental data presented in Fig. 18.5 illustrates the relationship between increases in carotid sinus pressure and changes in sympathetic efferent nerve activity and cardiac vagal nerve activity. The findings show that as carotid sinus pressure increases, sympathetic efferent nerve activity decreases and cardiac vagal nerve activity increases.

Fig. 18.6 demonstrates that intravenous infusions of blood or electrolyte solutions have opposing effects on heart rate. These infusions tend to increase heart rate through the Bainbridge reflex and decrease heart rate through the baroreceptor reflex. The actual change in heart rate induced by these infusions is the result of these two opposing effects.

Stimulation of the atrial receptors not only increases heart rate but also urine volume. This diuresis can be partially attributed to reduced activity in the renal sympathetic nerve fibers. However, the main mechanism involves a neural reduction in vasopressin secretion by the posterior pituitary gland. Stretch of the atrial walls also leads to the release of atrial natriuretic peptide (ANP) from the atria.

ANP, a 28–amino acid peptide, exerts diuretic and natriuretic effects on the kidneys and vasodilator effects on resistance and capacitance vessels. Thus, ANP plays a crucial role in regulating blood volume and blood pressure.

In congestive heart failure, the retention of sodium chloride and water occurs due to increased release of aldosterone from the adrenal cortex stimulated by the renin-angiotensin system. Additionally, the plasma level of ANP is elevated in congestive heart failure. By enhancing the renal excretion of sodium chloride and water, ANP gradually reduces fluid retention and consequent elevations in central venous pressure and cardiac preload.

Rhythmic variations in heart rate, occurring at the frequency of respiration, are commonly observed. These variations are more pronounced in children. Typically, heart rate accelerates during inspiration and decelerates during expiration (Fig. 18.7).

Myocytes of the ventricles secrete a related peptide known as brain natriuretic peptide (BNP) in response to stretch. BNP, initially discovered in the central nervous system, exerts actions similar to those of ANP (see Fig. 18.7).

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•Fig. 18.5 Experimentaldatashowingthatincreasesincarotidsinuspressureresultindecreasedsympatheticefferentnerve(Symp)activityandincreasedcardiacvagalnerveactivity.(AdaptedfromKollaiM,KoizumiK.Pflügers Arch. 1989;413:365.)100 50 0 60 100 140 180 220 Sinus pressure (mm Hg) Vagal activity (% of max) 100 50 0 Symp. activity (% of max) •Fig. 18.6 Intravenous Infusions of Blood or Electrolyte Solutions Tend to Increase the Heart Rate Through the Bainbridge Reflex and to Decrease the Heart Rate Through the Baroreceptor Reflex. Theactualchangeinheartrateinducedbysuchinfusionsistheresultofthesetwoopposingeffects.Intravenous infusion Increases right atrial pressure Atrial receptors stimulated Bainbridge reflex – + Increases cardiac output Increases arterial pressure Baroreceptor reflex Heart rate
Stimulation of the atrial receptors increases not only the heart rate but also urine volume. Reduced activity in the renal sympathetic nerve fibers may partially account for this diuresis. However, the principal mechanism appears to be a neurally mediated reduction in vasopressin (antidiuretic hormone) secretion by the posterior pituitary gland (see ). Stretch of the atrial walls also releases atrial natriuretic peptide (ANP) from the atria.
ANP, a 28–amino acid peptide, exerts potent diuretic and natriuretic effects on the kidneys (see also ) and vasodilator effects on the resistance and capacitance vessels. Thus ANP is an important regulator of blood volume and blood pressure.
Incongestiveheartfailure,NaClandwaterareretained,mainlybecausestimulationbytherenin-angiotensinsystemincreasesthereleaseofaldosteronefromtheadrenalcortex.TheplasmalevelofANPisalsoincreasedincongestiveheartfailure.ByenhancingtherenalexcretionofNaClandwater,ANPgraduallyreducesfluidretentionandtheconsequentelevationsincentralvenouspressureandcardiacpreload.
Rhythmic variations in heart rate, occurring at the frequency of respiration, are detectable in most individuals and tend to be more pronounced in children. The heart rate typically accelerates during inspiration and decelerates during expiration (Fig. 18.7 *The myocytes of the ventricles secrete a related peptide in response to stretch. This peptide, termed brain natriuretic peptide (BNP) because of its initial discovery in the central nervous system, has actions similar to those of ANP (see •Fig. 18.7 Respiratory Sinus Arrhythmia. Notethattheheartrateincreasesduringinspirationanddecreasesduringexpiration.(ModifiedfromWarnerMR,etal.Am J Physiol. 1986;251:H1134.)50 80 110 140 Expiration Time (sec) Inspiration 3 6 9 12 150 Heart rate(beats/min)