Page 145 - 84 human physiolofy part-1

The Cardiovascular System

Norepinephrine (noradrenaline) is released by the terminal boutons of depolarized sympathetic
fibers, at the sinoatrial and atrioventricular nodes. Norepinephrine diffuses across the synaptic cleft
binds to the β1-adrenoreceptors – G-protein linked receptors, consisting of seven transmembrane
domains – shifting their equilibrium towards the active state. The receptor changes its conformation
and mechanically activates the G-protein which is released. The G-protein is involved in the production
of cyclic adenyl monophosphate (camp) from adenosine triphosphate (ATP) and this in turn activates
the protein kinase (β-adrenoreceptor kinase). β-adrenoreceptor kinase phosphorylates the calcium ion
channels in the sarcolema, so that calcium ion influx is increased when they are activated by the
appropriate transmembrane voltage. This will of course, cause more of the calcium receptors in the
sarcoplasmic reticulum to be activated, creating a larger flow of calcium ions into the sarcoplasm.
More troponin will be bound and more myosin binding sites cleared [of tropomyosin] so that more
myosin heads can be recruited for the contraction and a greater force and speed of contraction results.
[Phosphodiesterase catalyses the decomposition of cAMP to AMP so that it is no longer able to activate
the protein kinase. AMP will of course, go on to be phosphorylated to ATP and may be recycled.]
Noradrenaline also affects the atrioventricular node, reducing the delay before continuing conduction
of the action potential via the bundle of HIS.

Diastole

The heart in the diastole phase. Cardiac Diastole is the period of time when the heart relaxes after
contraction in preparation for refilling with circulating blood. Ventricular diastole is when the
ventricles are relaxing, while atrial diastole is when the atria are relaxing. Together they are known as
complete cardiac diastole. During ventricular diastole, the pressure in the (left and right) ventricles
drops from the peak that it reaches in systole. When the pressure in the left ventricle drops to below the
pressure in the left atrium, the mitral valve opens, and the left ventricle fills with blood that was
accumulating in the left atrium. Likewise, when the pressure in the right ventricle drops below that in
the right atrium, the tricuspid valve opens and the right ventricle fills with blood that was in the right
atrium

"Lub-Dub"

The first heart tone, or S1, "Lub" is caused by the closure of the atrioventricular valves, mitral and
tricuspid, at the beginning of ventricular contraction, or systole. When the pressure in the ventricles
rises above the pressure in the atria, these valves close to prevent regurgitation of blood from the
ventricles into the atria. The second heart tone, or S2 (A2 and P2), "Dub" is caused by the closure of
the aortic valve and pulmonic valve at the end of ventricular systole. As the left ventricle empties, its
pressure falls below the pressure in the aorta, and the aortic valve closes. Similarly, as the pressure in
the right ventricle falls below the pressure in the pulmonary artery, the pulmonic valve closes. During
inspiration, negative intrathoracic pressure causes increased blood return into the right side of the heart.
The increased blood volume in the right ventricle causes the pulmonic valve to stay open longer during
ventricular systole. This causes an increased delay in the P2 component of S2. During expiration, the
positive intrathoracic pressure causes decreased blood return to the right side of the heart. The reduced
volume in the right ventricle allows the pulmonic valve to close earlier at the end of ventricular systole,
causing P2 to occur earlier, and "closer" to A2. It is physiological to hear the splitting of the second
heart tone by younger people and during inspiration. During expiration normally the interval between
the two components shortens and the tone becomes merged.

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