Same receptors, affinity is the same, binding is the same.

No one knows why Summary: para blocked more effectively than the sympathetic actions in all areas except the CV system. Except for CV -Parasympathetic is more potently inhibited -Sympathetic will usually be expressed except for heart -Sweating is only sympathetic. Lack of sweating because sympathetic is blocked too but not para part For male genital tract - impotence, neither erection or ejaculation can occur In CV system: Parasympathetic effects: decreased contractibility Sympathetic: relaxed arterioles (block sympathetic so no input to restrict) In patient with asthma (constricted bronchioles is treated with ganglionic blocker, what would happen? ASTHMA WOULD GET BETTER Distance between 2 sites for Ach binding at NMJ is wider than the q2 site for ch binding in the ganglion Patient would have amotile gut not diarrhea The bronchioles would have fewer blockages of SNS so bronchioles would dilate and the asthma would get better Cardiovascular effects of ganglionic blockers -Whens its most relaxed it fills up with blood In systole, when heart contracts, blood is forced out of left ventricle under high pressure At max contraction, it has the least amount of blood blood pressure is the pressure in the arteries ahtte maximum point of contraction of left ventricle over the pressure in the artiers when the left ventricle/right atrium is fully relaxed (systole over diastole) CO- vol of blood pumped from heart in one minte (normal is 5 liters/minute) Stroke volume - how much blood pumped out of heart in one contraction (heart beat) Stroke volume = end diastolic volume minus end systolic volume BP proportional to [peripheral resistance times CO Vasoconstriction - increased ressitance increased BP if CO is constant CO increases (running) and ressitant is same increased BP Not tested on Frank starling law - the greater the end diastolic volume, the greater stroke volume The more blood that gets into right atrium when its relaxed, the more blood is can pump

No para effect on peripheral blood vessels , but blocked sympathetic stimulation of arterioles causes relaxation and resistance drops giving a drop in blood pressure Ganglionic blockers have greater sympathetic effect in CV system so heart race and force decrease so GP decreased more When ganglionic blocker is given, the CV system cannot respond with appropriate reflexes and orthostatic hypotension occurs 1. relaexes blood vessels 2. blood pools in legs in a uprgith so less blood si retruend to heart and the EDV is rduced 3. EDV decreased leads to decerad storke volume 4. Decreased sympstahteic input directly to heart so that contracitlit decreases (inotropic effect) 5. Decreased stroke volume leasds tod ec Moajr side effect of treatment with ganglionic blockers is postural hhupotnesion QUESTION: a heltahy man is an car accident and has internal injuries and he primar ijury being a tron inferior vena cava. Thus venus retrun ot he right atrium is decreased. What will happen to his cardioutac out put in resosne tothis injury And what will happen to heart rate Decrease in CO, (EDV decreasesed, so SVdecreaes , and CO = SV times HR) Heart rate will increase in respoinse to drop in BP Decreased BP sensed by barorecetporsand firing of those receptors decrease What if victim was trying an ew drug to control his BP that was a ganglionic blocker. Given the decreased return to the heart what wll his heart rate and BP do in response to the deceraed cardiac ooutput BP will continue to drop as he blelds . when signal reaches the gangil it stops and the heart rate and blod pressure cannot increase . signal Effect of vasonconstriction on CV reflexes Normal: causes increased BP and impulse goes from carotid sinus to cardio reflex center and through the the vagus nerve to the AV node so there is decreased HR. simultaneous dereaed in sitmulation of he heart via sympathetic neurons. Pretreat with ganglionic blocker: heart rate stays the same because both para and sym are blocked Canoot measure the difference between when BP increase and heart rate drops Effect of vasodilator: normal : Bp falls, and increase in heart rate Pretreat with ganglionic blocker: BP falls , but reflexi s blcoekdand HR stays the same Ganglionic stimulator: Nicotine: binds sto noicotnic recetpos in thboth autonomic ganaglia and NMJ

Nictotine - causes diarrhea, salivation, hypertension, skeletal muscle fasiciculations Muscariini agonist: diarrhea, salviation ChE inhibitor: diarrhea, salviation, skeleteal muscle fasiculations If pt treated with ganglionic blocker and given direct acting vasodilator, BP - decreases HR - stays the same If pt not reated with ganglionic locker and then given direct acting vasoconstricter BP - increased HR - decreased Low dose nicotine stimulates an increase in Ach relsease in postganglionic parasympathaetic neurson Low doose nicotine sitmulates an increase in norepinephrine relsease in postganglionic sympathetic neurons At high dose - nicotine causes a depolarization blockand decrease Ach and norepinperprine secretion. Nicotine - parasympathetic effect overriding sympathetic effect, but for CV its flipped