control of blood pressure

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Topic:Control of Blood pressureMd.Jabiur RahamanDaffodil International UniversityDept. Of pharmacyControl of blood pressureMean blood pressure is controlled by changing total peripheral resistance and or cardiac output.

Cardiac output is controlled by sympathetic and para sympathetic nerves which effect:heart rateforce of contraction

TPR controlled by nervous and chemical means to effect constriction/dilatation ofarterioles and venules2Regulation of blood pressureHow is pressure measured?

Short termBaroreceptorsLong termKidney via renin angiotensin system3Location of baroreceptorsBaroreceptors sense stretch and rate of stretch by generating action potentials (voltage spikes)

Located in highly distensible regions of the circulation to maximise sensitivity

4Baroreceptor output(from single fibres)

Rapid decrease in mean pressureFrom: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)

Rapid increase in mean pressure

Response to pulse pressure5Two types of baroreceptorType AHigh sensitivityHigh firing rateType CLower sensitivityLower firing rateHigher threshold (before firing starts)Therefore can deal with higher pressures than type A which become saturatedFrom An Introduction to Cardiovascular PhysiologyJ.R. Levick

6Baroreceptor reflexBlood pressure fallsAortic archCarotid sinusConstriction of veins & arteriolesIncreased stroke volumeIncreased heartrateVasoconstrictionCardiac stimulationCardiac inhibitionNucleus tractus solitariusIncreased peripheral resistanceIncreased cardiac outputIncreased blood pressureNeural integrationSensorsEffectors7Other stretch receptorsCoronary artery baroreceptorsRespond to arterial pressure but more sensitive than carotid and aortic ones

Veno-atrial mechanoreceptorsRespond to changes in central blood volumeLie down, lift your legs and cause peripheral vasodilatation

Unmyelinated mechanoreceptorsRespond to distension of heartVentricular ones during systole; atrial ones during inspiration

8Other receptorsHeart chemosensorsCause pain in response to ischaemiaK+, lactic acid, bradykinin, prostaglandinsArterial chemosensorsStimulated in response toHypoxaemia, hypercapnia*, acidosis, hyperkalaemia**Regulate breathingLung stretch receptorsCause tachycardia during inspiration

*too much CO2**too much K+9Overview of short-term control mechanisms

From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)10Long term control of blood pressureInvolves control of blood volume/sodium balance by the kidneysHormonal controlRenin-angiotensin-aldosterone systemAntidiuretic hormone (vasopressin)Atrial natiuretic peptidePressure natriuresis11ArteriesVeinsReduced renalblood flowJuxtaglomerularapparatusReninAngiotensinogenAngiotensin IAngiotensin IIIncreasedpre-loadIncreasedafter-loadvasoconstrictionIncreased aldosteronesecretionSodium retentionFluid re-absorptionIncreasedblood volumeRenin/angiotensin/ aldosterone systemLV filling pressure)(LV pressurebeginning of systole)Increased blood volume in the thorax12Atrial natiuretic peptideIncreases salt excretion via kidneysBy reducing water reabsorption in the collecting ductsrelaxes renal arteriolesinhibits sodium reabsorption in the distal tubule

Released in response to stimulation of atrial receptors13Effect of blood lossless than 10%, no serious symptomse.g. blood transfusion20 - 30% blood loss not usually life threateninggreater than 30%, severe drop in BP and, often, death due to impaired cerebral and coronary perfusion