Contraction of cardiac muscle The increase in Ca++ in the cell causes muscle contraction (but we’ll pick up the rest of the story when we get to the muscular system).

Control of heart rate SNS releases norepinephrine on pacemaker cells--> HR by increasing the rate of depolarization by decreasing K+ permeability of pacemaker cells--therefore, cell less negative and it takes less time to reach threshold

Control of heart rate PNS releases acetylcholine on the pacemaker --> HR by decreasing the rate of depolarization by increasing the K+ permeability of pacemaker cells--therefore, cell more negative and it takes longer to reach threshold

Cardiovascular disease [includes heart disease (myocardial infarction) and stroke] What were top 3 causes of adult deaths in 1900? What were top 3 causes of adult deaths in 1990?

Women 50% more likely to die from heart disease than men Women 50% more likely to die from heart disease than men. 38% of women (vs. 25% of men) will die within one year of a recognized heart attack 35% of women (vs. 18% of men) heart attack survivors will have another heart attack within 6 years

Cholesterol Sources: liver and diet Uses in body: molecule from which steroid hormones and bile manufactured, component of cell membranes Transport in blood: high density lipoproteins (HDL) low density lipoproteins (LDL) (not VLDL--those are chylomicrons)

Athlerosclerosis (atheromas (smooth muscle cell proliferation)+sclerosis (proliferation of fibrous connective tissue) 1. Injury to artery wall by invasion of LDLs, oxidized cholesterol, free radicals, high blood pressure, chemicals from fat cells, or bacterial-induced inflammation. 2. Endothelial cells recruit WBCs to site 3. WBCs attack LDL site and form fatty streak 4. Proliferation of smooth muscle cells and fibrous connective tissue 5. Ca++ deposited and “hardens” vessel 6. Plaque= LDL, muscle cells, fibrous tissue, Ca++, WBCs

So… Artery less distensible due to plaque: 1 So… Artery less distensible due to plaque: 1. Reduced ability to produce nitric oxide 2. Ca++ makes plaque hard 3. Fibrous tissue less distensible than normal And… 1. Blockage can reduce or cut off blood flow 2. Plaque’s rough edges can stimulate clot formation

Athlerosclerosis: Starts early in life 20-30% of US soldiers killed in Viet Nam (ages 18-32) had 20-30% blockage of coronary arteries 1991 survey by Wardenburg showed that 13% of CU undergraduates had seriously high cholesterol US children now showing blockages similar to 40-yr olds--heart attacks likely

BLOOD PRESSURE Flow rate = P x radius of vessel4 BLOOD PRESSURE Flow rate = P x radius of vessel4 length x   = viscosity (function of number of red blood cells and concentration of plasma proteins)

Blood pressure = cardiac output x peripheral resistance Cardiac output = heart rate x stroke volume Peripheral resistance = degree of vasoconstriction or vasodilation of arterioles

Cardiac output Heart rate  by SNS.  by PNS Stroke volume Cardiac output Heart rate  by SNS  by PNS Stroke volume venous return  by SNS strength of contraction  by SNS

Peripheral resistance  by SNS output  by  SNS output

Regulation of blood pressure Sensors: 1. baroreceptors and 2 Regulation of blood pressure Sensors: 1. baroreceptors and 2. chemoreceptors in aorta and carotid 3. medulla itself Integrator: medulla vasomotor center Output: PNS and SNS

 BP --> sensors --> medulla -->  PNS-->  heart rate  SNS-->  heart rate  venous return -->stroke volume  peripheral resistance   BP

 BP --> sensors --> medulla -->  PNS-->  heart rate SNS-->  heart rate  venous return --> stroke volume  peripheral resistance   BP

And…. BP --> kidney (sensor and integrator)--> renin--> renin converts angiotensinogen to angiotensin I--which is converted to--> angiotensin II by lung converting enzyme-> angiotensin II causes: 1.vasoconstriction --  peripheral resistance 2. reduces GFR --> kidney reduces urine production-> blood volume  -->  venous return -->  stroke volume 3. Stimulates thirst-->  blood volume -->  venous return --->  stroke volume and ….. 

Angiotensin II also causes:  aldosterone release from adrenal gland --->  Na+ uptake from urine -->  water uptake from urine -->  blood volume -->  venous return --> stroke volume -->  cardiac output net effect of  angiotensin II -->  BP

Circulatory Shock 1. Hypovolemic 2. Cardiogenic 3. Vasogenic 4 Circulatory Shock 1. Hypovolemic 2. Cardiogenic 3. Vasogenic 4. Neurogenic

Shock (due to loss of blood) = low BP Non-progressive--can recover with massive SNS output and renin-angiotensin (later need to restore RBC’s) Progressive--positive feedback BP -->  flow --> BP --> flow …  flow leads to  BP because of lack of adequate oxygen to medulla, which loses control of SNS

Hypertension  peripheral resistance due to athlerosclerosis  aldosterone secretion  renin secretion neurogenic “essential hypertension”

Local control over blood flow Medulla/SNS always takes priority over local needs

Exercise Input from higher centers causes Medulla/SNS to change distribution of blood and change in BP regulation